CD147-induced cell proliferation is associated with Smad4 signal inhibition
CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Sma...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Qin, Hui [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
11 |
|---|
| Übergeordnetes Werk: |
Enthalten in: 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS - 2012, ECR, Orlando, Fla |
|---|---|
| Übergeordnetes Werk: |
volume:358 ; year:2017 ; number:2 ; day:15 ; month:09 ; pages:279-289 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.yexcr.2017.07.003 |
|---|
| Katalog-ID: |
ELV036167819 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV036167819 | ||
| 003 | DE-627 | ||
| 005 | 20230625211113.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2017 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.yexcr.2017.07.003 |2 doi | |
| 028 | 5 | 2 | |a GBV00000000000431.pica |
| 035 | |a (DE-627)ELV036167819 | ||
| 035 | |a (ELSEVIER)S0014-4827(17)30355-5 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | 4 | |a 610 |q VZ |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.44 |2 bkl | ||
| 100 | 1 | |a Qin, Hui |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a CD147-induced cell proliferation is associated with Smad4 signal inhibition |
| 264 | 1 | |c 2017transfer abstract | |
| 300 | |a 11 | ||
| 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 CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. | ||
| 520 | |a CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. | ||
| 650 | 7 | |a CD147-ICD |2 Elsevier | |
| 650 | 7 | |a PMSF |2 Elsevier | |
| 650 | 7 | |a FBS |2 Elsevier | |
| 650 | 7 | |a TGF-β |2 Elsevier | |
| 650 | 7 | |a PFA |2 Elsevier | |
| 650 | 7 | |a CD147 |2 Elsevier | |
| 650 | 7 | |a PCa |2 Elsevier | |
| 700 | 1 | |a Rasul, Azhar |4 oth | |
| 700 | 1 | |a Li, Xin |4 oth | |
| 700 | 1 | |a Masood, Muqaddas |4 oth | |
| 700 | 1 | |a Yang, Guang |4 oth | |
| 700 | 1 | |a Wang, Na |4 oth | |
| 700 | 1 | |a Wei, Wei |4 oth | |
| 700 | 1 | |a He, Xi |4 oth | |
| 700 | 1 | |a Watanabe, Nobumoto |4 oth | |
| 700 | 1 | |a Li, Jiang |4 oth | |
| 700 | 1 | |a Li, Xiaomeng |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Academic Press |t 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |d 2012 |d ECR |g Orlando, Fla |w (DE-627)ELV011050691 |
| 773 | 1 | 8 | |g volume:358 |g year:2017 |g number:2 |g day:15 |g month:09 |g pages:279-289 |g extent:11 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.yexcr.2017.07.003 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 912 | |a GBV_ILN_70 | ||
| 936 | b | k | |a 44.44 |j Parasitologie |x Medizin |q VZ |
| 951 | |a AR | ||
| 952 | |d 358 |j 2017 |e 2 |b 15 |c 0915 |h 279-289 |g 11 | ||
| author_variant |
h q hq |
|---|---|
| matchkey_str |
qinhuirasulazharlixinmasoodmuqaddasyangg:2017----:d4idcdelrlfrtoiascaewtsa |
| hierarchy_sort_str |
2017transfer abstract |
| bklnumber |
44.44 |
| publishDate |
2017 |
| allfields |
10.1016/j.yexcr.2017.07.003 doi GBV00000000000431.pica (DE-627)ELV036167819 (ELSEVIER)S0014-4827(17)30355-5 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Qin, Hui verfasserin aut CD147-induced cell proliferation is associated with Smad4 signal inhibition 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa Elsevier Rasul, Azhar oth Li, Xin oth Masood, Muqaddas oth Yang, Guang oth Wang, Na oth Wei, Wei oth He, Xi oth Watanabe, Nobumoto oth Li, Jiang oth Li, Xiaomeng oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 https://doi.org/10.1016/j.yexcr.2017.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 358 2017 2 15 0915 279-289 11 |
| spelling |
10.1016/j.yexcr.2017.07.003 doi GBV00000000000431.pica (DE-627)ELV036167819 (ELSEVIER)S0014-4827(17)30355-5 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Qin, Hui verfasserin aut CD147-induced cell proliferation is associated with Smad4 signal inhibition 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa Elsevier Rasul, Azhar oth Li, Xin oth Masood, Muqaddas oth Yang, Guang oth Wang, Na oth Wei, Wei oth He, Xi oth Watanabe, Nobumoto oth Li, Jiang oth Li, Xiaomeng oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 https://doi.org/10.1016/j.yexcr.2017.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 358 2017 2 15 0915 279-289 11 |
| allfields_unstemmed |
10.1016/j.yexcr.2017.07.003 doi GBV00000000000431.pica (DE-627)ELV036167819 (ELSEVIER)S0014-4827(17)30355-5 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Qin, Hui verfasserin aut CD147-induced cell proliferation is associated with Smad4 signal inhibition 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa Elsevier Rasul, Azhar oth Li, Xin oth Masood, Muqaddas oth Yang, Guang oth Wang, Na oth Wei, Wei oth He, Xi oth Watanabe, Nobumoto oth Li, Jiang oth Li, Xiaomeng oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 https://doi.org/10.1016/j.yexcr.2017.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 358 2017 2 15 0915 279-289 11 |
| allfieldsGer |
10.1016/j.yexcr.2017.07.003 doi GBV00000000000431.pica (DE-627)ELV036167819 (ELSEVIER)S0014-4827(17)30355-5 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Qin, Hui verfasserin aut CD147-induced cell proliferation is associated with Smad4 signal inhibition 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa Elsevier Rasul, Azhar oth Li, Xin oth Masood, Muqaddas oth Yang, Guang oth Wang, Na oth Wei, Wei oth He, Xi oth Watanabe, Nobumoto oth Li, Jiang oth Li, Xiaomeng oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 https://doi.org/10.1016/j.yexcr.2017.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 358 2017 2 15 0915 279-289 11 |
| allfieldsSound |
10.1016/j.yexcr.2017.07.003 doi GBV00000000000431.pica (DE-627)ELV036167819 (ELSEVIER)S0014-4827(17)30355-5 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Qin, Hui verfasserin aut CD147-induced cell proliferation is associated with Smad4 signal inhibition 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa Elsevier Rasul, Azhar oth Li, Xin oth Masood, Muqaddas oth Yang, Guang oth Wang, Na oth Wei, Wei oth He, Xi oth Watanabe, Nobumoto oth Li, Jiang oth Li, Xiaomeng oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 https://doi.org/10.1016/j.yexcr.2017.07.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 358 2017 2 15 0915 279-289 11 |
| language |
English |
| source |
Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 |
| sourceStr |
Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:358 year:2017 number:2 day:15 month:09 pages:279-289 extent:11 |
| format_phy_str_mv |
Article |
| bklname |
Parasitologie |
| institution |
findex.gbv.de |
| topic_facet |
CD147-ICD PMSF FBS TGF-β PFA CD147 PCa |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
| authorswithroles_txt_mv |
Qin, Hui @@aut@@ Rasul, Azhar @@oth@@ Li, Xin @@oth@@ Masood, Muqaddas @@oth@@ Yang, Guang @@oth@@ Wang, Na @@oth@@ Wei, Wei @@oth@@ He, Xi @@oth@@ Watanabe, Nobumoto @@oth@@ Li, Jiang @@oth@@ Li, Xiaomeng @@oth@@ |
| publishDateDaySort_date |
2017-01-15T00:00:00Z |
| hierarchy_top_id |
ELV011050691 |
| dewey-sort |
3610 |
| id |
ELV036167819 |
| 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">ELV036167819</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625211113.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.yexcr.2017.07.003</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000431.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV036167819</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4827(17)30355-5</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="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.44</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Qin, Hui</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CD147-induced cell proliferation is associated with Smad4 signal inhibition</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</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">CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD147-ICD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PMSF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">FBS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TGF-β</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PFA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD147</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PCa</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rasul, Azhar</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Xin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Masood, Muqaddas</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Guang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Na</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wei, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Xi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Watanabe, Nobumoto</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Jiang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Xiaomeng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="t">72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS</subfield><subfield code="d">2012</subfield><subfield code="d">ECR</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV011050691</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:358</subfield><subfield code="g">year:2017</subfield><subfield code="g">number:2</subfield><subfield code="g">day:15</subfield><subfield code="g">month:09</subfield><subfield code="g">pages:279-289</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.yexcr.2017.07.003</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">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.44</subfield><subfield code="j">Parasitologie</subfield><subfield code="x">Medizin</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">358</subfield><subfield code="j">2017</subfield><subfield code="e">2</subfield><subfield code="b">15</subfield><subfield code="c">0915</subfield><subfield code="h">279-289</subfield><subfield code="g">11</subfield></datafield></record></collection>
|
| author |
Qin, Hui |
| spellingShingle |
Qin, Hui ddc 610 bkl 44.44 Elsevier CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa CD147-induced cell proliferation is associated with Smad4 signal inhibition |
| authorStr |
Qin, Hui |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV011050691 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 VZ 44.44 bkl CD147-induced cell proliferation is associated with Smad4 signal inhibition CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa Elsevier |
| topic |
ddc 610 bkl 44.44 Elsevier CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa |
| topic_unstemmed |
ddc 610 bkl 44.44 Elsevier CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa |
| topic_browse |
ddc 610 bkl 44.44 Elsevier CD147-ICD Elsevier PMSF Elsevier FBS Elsevier TGF-β Elsevier PFA Elsevier CD147 Elsevier PCa |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
a r ar x l xl m m mm g y gy n w nw w w ww x h xh n w nw j l jl x l xl |
| hierarchy_parent_title |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
| hierarchy_parent_id |
ELV011050691 |
| dewey-tens |
610 - Medicine & health |
| hierarchy_top_title |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV011050691 |
| title |
CD147-induced cell proliferation is associated with Smad4 signal inhibition |
| ctrlnum |
(DE-627)ELV036167819 (ELSEVIER)S0014-4827(17)30355-5 |
| title_full |
CD147-induced cell proliferation is associated with Smad4 signal inhibition |
| author_sort |
Qin, Hui |
| journal |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
| journalStr |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2017 |
| contenttype_str_mv |
zzz |
| container_start_page |
279 |
| author_browse |
Qin, Hui |
| container_volume |
358 |
| physical |
11 |
| class |
610 VZ 44.44 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Qin, Hui |
| doi_str_mv |
10.1016/j.yexcr.2017.07.003 |
| dewey-full |
610 |
| title_sort |
cd147-induced cell proliferation is associated with smad4 signal inhibition |
| title_auth |
CD147-induced cell proliferation is associated with Smad4 signal inhibition |
| abstract |
CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. |
| abstractGer |
CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. |
| abstract_unstemmed |
CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 |
| container_issue |
2 |
| title_short |
CD147-induced cell proliferation is associated with Smad4 signal inhibition |
| url |
https://doi.org/10.1016/j.yexcr.2017.07.003 |
| remote_bool |
true |
| author2 |
Rasul, Azhar Li, Xin Masood, Muqaddas Yang, Guang Wang, Na Wei, Wei He, Xi Watanabe, Nobumoto Li, Jiang Li, Xiaomeng |
| author2Str |
Rasul, Azhar Li, Xin Masood, Muqaddas Yang, Guang Wang, Na Wei, Wei He, Xi Watanabe, Nobumoto Li, Jiang Li, Xiaomeng |
| ppnlink |
ELV011050691 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.yexcr.2017.07.003 |
| up_date |
2024-07-06T19:29:12.029Z |
| _version_ |
1803859160760057856 |
| 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">ELV036167819</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625211113.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.yexcr.2017.07.003</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000431.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV036167819</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4827(17)30355-5</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="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.44</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Qin, Hui</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CD147-induced cell proliferation is associated with Smad4 signal inhibition</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</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">CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21WAF1. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21WAF1 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD147-ICD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PMSF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">FBS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TGF-β</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PFA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD147</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PCa</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rasul, Azhar</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Xin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Masood, Muqaddas</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Guang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Na</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wei, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Xi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Watanabe, Nobumoto</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Jiang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Xiaomeng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="t">72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS</subfield><subfield code="d">2012</subfield><subfield code="d">ECR</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV011050691</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:358</subfield><subfield code="g">year:2017</subfield><subfield code="g">number:2</subfield><subfield code="g">day:15</subfield><subfield code="g">month:09</subfield><subfield code="g">pages:279-289</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.yexcr.2017.07.003</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">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.44</subfield><subfield code="j">Parasitologie</subfield><subfield code="x">Medizin</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">358</subfield><subfield code="j">2017</subfield><subfield code="e">2</subfield><subfield code="b">15</subfield><subfield code="c">0915</subfield><subfield code="h">279-289</subfield><subfield code="g">11</subfield></datafield></record></collection>
|
| score |
7.3998823 |