The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth
Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial gr...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Nakamura, Mitsuhiro [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
8 |
|---|
| Übergeordnetes Werk: |
Enthalten in: GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome - Hao, Lijun ELSEVIER, 2015, an international journal providing a forum for original and pertinent contributions in cancer research, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:336 ; year:2013 ; number:1 ; day:9 ; month:08 ; pages:68-75 ; extent:8 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.canlet.2013.04.010 |
|---|
| Katalog-ID: |
ELV033073791 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV033073791 | ||
| 003 | DE-627 | ||
| 005 | 20230625192845.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2013 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.canlet.2013.04.010 |2 doi | |
| 028 | 5 | 2 | |a GBVA2013010000010.pica |
| 035 | |a (DE-627)ELV033073791 | ||
| 035 | |a (ELSEVIER)S0304-3835(13)00330-3 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 570 | |
| 082 | 0 | 4 | |a 570 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 082 | 0 | 4 | |a 600 |a 690 |q VZ |
| 084 | |a 51.00 |2 bkl | ||
| 084 | |a 51.32 |2 bkl | ||
| 100 | 1 | |a Nakamura, Mitsuhiro |e verfasserin |4 aut | |
| 245 | 1 | 4 | |a The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| 264 | 1 | |c 2013transfer abstract | |
| 300 | |a 8 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. | ||
| 520 | |a Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. | ||
| 650 | 7 | |a Endometrial epithelial cell |2 Elsevier | |
| 650 | 7 | |a IGFBP-1 |2 Elsevier | |
| 650 | 7 | |a Progestin |2 Elsevier | |
| 650 | 7 | |a Growth inhibition |2 Elsevier | |
| 650 | 7 | |a FOXO1 |2 Elsevier | |
| 700 | 1 | |a Takakura, Masahiro |4 oth | |
| 700 | 1 | |a Fujii, Reina |4 oth | |
| 700 | 1 | |a Maida, Yoshiko |4 oth | |
| 700 | 1 | |a Bono, Yukiko |4 oth | |
| 700 | 1 | |a Mizumoto, Yasunari |4 oth | |
| 700 | 1 | |a Zhang, Xian |4 oth | |
| 700 | 1 | |a Kiyono, Tohru |4 oth | |
| 700 | 1 | |a Kyo, Satoru |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Hao, Lijun ELSEVIER |t GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome |d 2015 |d an international journal providing a forum for original and pertinent contributions in cancer research |g Amsterdam [u.a.] |w (DE-627)ELV013094742 |
| 773 | 1 | 8 | |g volume:336 |g year:2013 |g number:1 |g day:9 |g month:08 |g pages:68-75 |g extent:8 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.canlet.2013.04.010 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a GBV_ILN_11 | ||
| 912 | |a GBV_ILN_40 | ||
| 936 | b | k | |a 51.00 |j Werkstoffkunde: Allgemeines |q VZ |
| 936 | b | k | |a 51.32 |j Werkstoffmechanik |q VZ |
| 951 | |a AR | ||
| 952 | |d 336 |j 2013 |e 1 |b 9 |c 0809 |h 68-75 |g 8 | ||
| 953 | |2 045F |a 570 | ||
| author_variant |
m n mn |
|---|---|
| matchkey_str |
nakamuramitsuhirotakakuramasahirofujiire:2013----:hpbeednfx1gb1xsssetafrrgsitihbtno |
| hierarchy_sort_str |
2013transfer abstract |
| bklnumber |
51.00 51.32 |
| publishDate |
2013 |
| allfields |
10.1016/j.canlet.2013.04.010 doi GBVA2013010000010.pica (DE-627)ELV033073791 (ELSEVIER)S0304-3835(13)00330-3 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Nakamura, Mitsuhiro verfasserin aut The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth 2013transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 Elsevier Takakura, Masahiro oth Fujii, Reina oth Maida, Yoshiko oth Bono, Yukiko oth Mizumoto, Yasunari oth Zhang, Xian oth Kiyono, Tohru oth Kyo, Satoru oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 https://doi.org/10.1016/j.canlet.2013.04.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 336 2013 1 9 0809 68-75 8 045F 570 |
| spelling |
10.1016/j.canlet.2013.04.010 doi GBVA2013010000010.pica (DE-627)ELV033073791 (ELSEVIER)S0304-3835(13)00330-3 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Nakamura, Mitsuhiro verfasserin aut The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth 2013transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 Elsevier Takakura, Masahiro oth Fujii, Reina oth Maida, Yoshiko oth Bono, Yukiko oth Mizumoto, Yasunari oth Zhang, Xian oth Kiyono, Tohru oth Kyo, Satoru oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 https://doi.org/10.1016/j.canlet.2013.04.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 336 2013 1 9 0809 68-75 8 045F 570 |
| allfields_unstemmed |
10.1016/j.canlet.2013.04.010 doi GBVA2013010000010.pica (DE-627)ELV033073791 (ELSEVIER)S0304-3835(13)00330-3 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Nakamura, Mitsuhiro verfasserin aut The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth 2013transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 Elsevier Takakura, Masahiro oth Fujii, Reina oth Maida, Yoshiko oth Bono, Yukiko oth Mizumoto, Yasunari oth Zhang, Xian oth Kiyono, Tohru oth Kyo, Satoru oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 https://doi.org/10.1016/j.canlet.2013.04.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 336 2013 1 9 0809 68-75 8 045F 570 |
| allfieldsGer |
10.1016/j.canlet.2013.04.010 doi GBVA2013010000010.pica (DE-627)ELV033073791 (ELSEVIER)S0304-3835(13)00330-3 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Nakamura, Mitsuhiro verfasserin aut The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth 2013transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 Elsevier Takakura, Masahiro oth Fujii, Reina oth Maida, Yoshiko oth Bono, Yukiko oth Mizumoto, Yasunari oth Zhang, Xian oth Kiyono, Tohru oth Kyo, Satoru oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 https://doi.org/10.1016/j.canlet.2013.04.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 336 2013 1 9 0809 68-75 8 045F 570 |
| allfieldsSound |
10.1016/j.canlet.2013.04.010 doi GBVA2013010000010.pica (DE-627)ELV033073791 (ELSEVIER)S0304-3835(13)00330-3 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Nakamura, Mitsuhiro verfasserin aut The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth 2013transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 Elsevier Takakura, Masahiro oth Fujii, Reina oth Maida, Yoshiko oth Bono, Yukiko oth Mizumoto, Yasunari oth Zhang, Xian oth Kiyono, Tohru oth Kyo, Satoru oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 https://doi.org/10.1016/j.canlet.2013.04.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 336 2013 1 9 0809 68-75 8 045F 570 |
| language |
English |
| source |
Enthalten in GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome Amsterdam [u.a.] volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 |
| sourceStr |
Enthalten in GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome Amsterdam [u.a.] volume:336 year:2013 number:1 day:9 month:08 pages:68-75 extent:8 |
| format_phy_str_mv |
Article |
| bklname |
Werkstoffkunde: Allgemeines Werkstoffmechanik |
| institution |
findex.gbv.de |
| topic_facet |
Endometrial epithelial cell IGFBP-1 Progestin Growth inhibition FOXO1 |
| dewey-raw |
570 |
| isfreeaccess_bool |
false |
| container_title |
GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome |
| authorswithroles_txt_mv |
Nakamura, Mitsuhiro @@aut@@ Takakura, Masahiro @@oth@@ Fujii, Reina @@oth@@ Maida, Yoshiko @@oth@@ Bono, Yukiko @@oth@@ Mizumoto, Yasunari @@oth@@ Zhang, Xian @@oth@@ Kiyono, Tohru @@oth@@ Kyo, Satoru @@oth@@ |
| publishDateDaySort_date |
2013-01-09T00:00:00Z |
| hierarchy_top_id |
ELV013094742 |
| dewey-sort |
3570 |
| id |
ELV033073791 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV033073791</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625192845.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.canlet.2013.04.010</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013010000010.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV033073791</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0304-3835(13)00330-3</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">600</subfield><subfield code="a">690</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">51.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">51.32</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Nakamura, Mitsuhiro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">8</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Endometrial epithelial cell</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IGFBP-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Progestin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Growth inhibition</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">FOXO1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Takakura, Masahiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fujii, Reina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Maida, Yoshiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bono, Yukiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mizumoto, Yasunari</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Xian</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kiyono, Tohru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kyo, Satoru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Hao, Lijun ELSEVIER</subfield><subfield code="t">GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome</subfield><subfield code="d">2015</subfield><subfield code="d">an international journal providing a forum for original and pertinent contributions in cancer research</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV013094742</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:336</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:1</subfield><subfield code="g">day:9</subfield><subfield code="g">month:08</subfield><subfield code="g">pages:68-75</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.canlet.2013.04.010</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">51.00</subfield><subfield code="j">Werkstoffkunde: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">51.32</subfield><subfield code="j">Werkstoffmechanik</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">336</subfield><subfield code="j">2013</subfield><subfield code="e">1</subfield><subfield code="b">9</subfield><subfield code="c">0809</subfield><subfield code="h">68-75</subfield><subfield code="g">8</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
|
| author |
Nakamura, Mitsuhiro |
| spellingShingle |
Nakamura, Mitsuhiro ddc 570 ddc 610 ddc 600 bkl 51.00 bkl 51.32 Elsevier Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| authorStr |
Nakamura, Mitsuhiro |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV013094742 |
| format |
electronic Article |
| dewey-ones |
570 - Life sciences; biology 610 - Medicine & health 600 - Technology 690 - Buildings |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 Elsevier |
| topic |
ddc 570 ddc 610 ddc 600 bkl 51.00 bkl 51.32 Elsevier Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 |
| topic_unstemmed |
ddc 570 ddc 610 ddc 600 bkl 51.00 bkl 51.32 Elsevier Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 |
| topic_browse |
ddc 570 ddc 610 ddc 600 bkl 51.00 bkl 51.32 Elsevier Endometrial epithelial cell Elsevier IGFBP-1 Elsevier Progestin Elsevier Growth inhibition Elsevier FOXO1 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
m t mt r f rf y m ym y b yb y m ym x z xz t k tk s k sk |
| hierarchy_parent_title |
GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome |
| hierarchy_parent_id |
ELV013094742 |
| dewey-tens |
570 - Life sciences; biology 610 - Medicine & health 600 - Technology 690 - Building & construction |
| hierarchy_top_title |
GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV013094742 |
| title |
The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| ctrlnum |
(DE-627)ELV033073791 (ELSEVIER)S0304-3835(13)00330-3 |
| title_full |
The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| author_sort |
Nakamura, Mitsuhiro |
| journal |
GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome |
| journalStr |
GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
500 - Science 600 - Technology |
| recordtype |
marc |
| publishDateSort |
2013 |
| contenttype_str_mv |
zzz |
| container_start_page |
68 |
| author_browse |
Nakamura, Mitsuhiro |
| container_volume |
336 |
| physical |
8 |
| class |
570 570 DE-600 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Nakamura, Mitsuhiro |
| doi_str_mv |
10.1016/j.canlet.2013.04.010 |
| dewey-full |
570 610 600 690 |
| title_sort |
prb-dependent foxo1/igfbp-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| title_auth |
The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| abstract |
Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. |
| abstractGer |
Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. |
| abstract_unstemmed |
Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 |
| container_issue |
1 |
| title_short |
The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth |
| url |
https://doi.org/10.1016/j.canlet.2013.04.010 |
| remote_bool |
true |
| author2 |
Takakura, Masahiro Fujii, Reina Maida, Yoshiko Bono, Yukiko Mizumoto, Yasunari Zhang, Xian Kiyono, Tohru Kyo, Satoru |
| author2Str |
Takakura, Masahiro Fujii, Reina Maida, Yoshiko Bono, Yukiko Mizumoto, Yasunari Zhang, Xian Kiyono, Tohru Kyo, Satoru |
| ppnlink |
ELV013094742 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.canlet.2013.04.010 |
| up_date |
2024-07-06T17:42:57.608Z |
| _version_ |
1803852476695183360 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV033073791</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625192845.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.canlet.2013.04.010</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013010000010.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV033073791</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0304-3835(13)00330-3</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">600</subfield><subfield code="a">690</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">51.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">51.32</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Nakamura, Mitsuhiro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The PRB-dependent FOXO1/IGFBP-1 axis is essential for progestin to inhibit endometrial epithelial growth</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">8</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Progestin inhibits the growth of normal and cancerous endometria via the progesterone receptor (PR), but the distinct functions and signalings of PR subtypes have not been fully understood. The aim of the present study was to dissect the key pathways of progestin to inhibit endometrial epithelial growth. Immortalized endometrial epithelial cells (EM-E6/E7/TERT) with stable PRA or PRB expression were established and used for the experiments. In vitro growth inhibition by progestin was mainly observed in EM-E6/E7/TERT cells with PRB rather than those with PRA. RT-PCR assay confirmed that FOXO1, a key gene for progestin action, was up-regulated by progestin in a PRB-dependent manner. cDNA microarray analysis identified IGFBP-1, which contains FOXO1 binding sites on its promoter, to be induced by medroxyprogesterone acetate (MPA) in EM-E6/E7/TERT cells with PRB but not with PRA. siRNA knockdown of FOXO1 disturbed the induction of IGFBP-1 by MPA, while IGFBP-1 knockdown showed no effect on MPA-induced FOXO1 expression, indicating that FOXO1 is an upstream regulator of IGFBP-1. Luciferase reporter assays showed that MPA activated the IGFBP-1 promoter, which was cancelled by FOXO1 knockdown. Chromatin immunoprecipitation assay confirmed the in vivo binding of FOXO1 to the core promoter of IGFBP-1. IGFBP-1 knockdown significantly attenuated the growth inhibitory effects of MPA. The FOXO1/IGFBP-1 axis is essential for PRB-dependent growth inhibition of endometrial epithelial cells, offering a potential therapeutic clue to enhance the progestin effect.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Endometrial epithelial cell</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IGFBP-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Progestin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Growth inhibition</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">FOXO1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Takakura, Masahiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fujii, Reina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Maida, Yoshiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bono, Yukiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mizumoto, Yasunari</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Xian</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kiyono, Tohru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kyo, Satoru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Hao, Lijun ELSEVIER</subfield><subfield code="t">GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome</subfield><subfield code="d">2015</subfield><subfield code="d">an international journal providing a forum for original and pertinent contributions in cancer research</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV013094742</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:336</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:1</subfield><subfield code="g">day:9</subfield><subfield code="g">month:08</subfield><subfield code="g">pages:68-75</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.canlet.2013.04.010</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">51.00</subfield><subfield code="j">Werkstoffkunde: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">51.32</subfield><subfield code="j">Werkstoffmechanik</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">336</subfield><subfield code="j">2013</subfield><subfield code="e">1</subfield><subfield code="b">9</subfield><subfield code="c">0809</subfield><subfield code="h">68-75</subfield><subfield code="g">8</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
|
| score |
7.4002647 |