FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer
We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between...
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Gespeichert in:
| Autor*in: |
Kamil Mieczkowski [verfasserIn] Kamila Kitowska [verfasserIn] Marcin Braun [verfasserIn] Barbara Galikowska‐Bogut [verfasserIn] Monika Gorska‐Arcisz [verfasserIn] Dominika Piasecka [verfasserIn] Konrad Stawiski [verfasserIn] Anna J. Zaczek [verfasserIn] Dariusz Nejc [verfasserIn] Radzisław Kordek [verfasserIn] Hanna M. Romanska [verfasserIn] Rafal Sadej [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Molecular Oncology - Wiley, 2017, 16(2022), 15, Seite 2823-2842 |
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| Übergeordnetes Werk: |
volume:16 ; year:2022 ; number:15 ; pages:2823-2842 |
| Links: |
Link aufrufen |
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| DOI / URN: |
10.1002/1878-0261.13274 |
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| Katalog-ID: |
DOAJ026387085 |
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| 520 | |a We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. | ||
| 650 | 4 | |a ER | |
| 650 | 4 | |a FGFR2 | |
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| 650 | 4 | |a luminal breast cancer | |
| 650 | 4 | |a PR | |
| 650 | 4 | |a steroid hormones | |
| 653 | 0 | |a Neoplasms. Tumors. Oncology. Including cancer and carcinogens | |
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| 700 | 0 | |a Marcin Braun |e verfasserin |4 aut | |
| 700 | 0 | |a Barbara Galikowska‐Bogut |e verfasserin |4 aut | |
| 700 | 0 | |a Monika Gorska‐Arcisz |e verfasserin |4 aut | |
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| 700 | 0 | |a Konrad Stawiski |e verfasserin |4 aut | |
| 700 | 0 | |a Anna J. Zaczek |e verfasserin |4 aut | |
| 700 | 0 | |a Dariusz Nejc |e verfasserin |4 aut | |
| 700 | 0 | |a Radzisław Kordek |e verfasserin |4 aut | |
| 700 | 0 | |a Hanna M. Romanska |e verfasserin |4 aut | |
| 700 | 0 | |a Rafal Sadej |e verfasserin |4 aut | |
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10.1002/1878-0261.13274 doi (DE-627)DOAJ026387085 (DE-599)DOAJdbc206886c77407899872ff4d501edb9 DE-627 ger DE-627 rakwb eng RC254-282 Kamil Mieczkowski verfasserin aut FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. ER FGFR2 JunB luminal breast cancer PR steroid hormones Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Marcin Braun verfasserin aut Barbara Galikowska‐Bogut verfasserin aut Monika Gorska‐Arcisz verfasserin aut Dominika Piasecka verfasserin aut Konrad Stawiski verfasserin aut Anna J. Zaczek verfasserin aut Dariusz Nejc verfasserin aut Radzisław Kordek verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Molecular Oncology Wiley, 2017 16(2022), 15, Seite 2823-2842 (DE-627)531199800 (DE-600)2322586-5 18780261 nnns volume:16 year:2022 number:15 pages:2823-2842 https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/article/dbc206886c77407899872ff4d501edb9 kostenfrei https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/toc/1574-7891 Journal toc kostenfrei https://doaj.org/toc/1878-0261 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2022 15 2823-2842 |
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10.1002/1878-0261.13274 doi (DE-627)DOAJ026387085 (DE-599)DOAJdbc206886c77407899872ff4d501edb9 DE-627 ger DE-627 rakwb eng RC254-282 Kamil Mieczkowski verfasserin aut FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. ER FGFR2 JunB luminal breast cancer PR steroid hormones Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Marcin Braun verfasserin aut Barbara Galikowska‐Bogut verfasserin aut Monika Gorska‐Arcisz verfasserin aut Dominika Piasecka verfasserin aut Konrad Stawiski verfasserin aut Anna J. Zaczek verfasserin aut Dariusz Nejc verfasserin aut Radzisław Kordek verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Molecular Oncology Wiley, 2017 16(2022), 15, Seite 2823-2842 (DE-627)531199800 (DE-600)2322586-5 18780261 nnns volume:16 year:2022 number:15 pages:2823-2842 https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/article/dbc206886c77407899872ff4d501edb9 kostenfrei https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/toc/1574-7891 Journal toc kostenfrei https://doaj.org/toc/1878-0261 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2022 15 2823-2842 |
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10.1002/1878-0261.13274 doi (DE-627)DOAJ026387085 (DE-599)DOAJdbc206886c77407899872ff4d501edb9 DE-627 ger DE-627 rakwb eng RC254-282 Kamil Mieczkowski verfasserin aut FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. ER FGFR2 JunB luminal breast cancer PR steroid hormones Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Marcin Braun verfasserin aut Barbara Galikowska‐Bogut verfasserin aut Monika Gorska‐Arcisz verfasserin aut Dominika Piasecka verfasserin aut Konrad Stawiski verfasserin aut Anna J. Zaczek verfasserin aut Dariusz Nejc verfasserin aut Radzisław Kordek verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Molecular Oncology Wiley, 2017 16(2022), 15, Seite 2823-2842 (DE-627)531199800 (DE-600)2322586-5 18780261 nnns volume:16 year:2022 number:15 pages:2823-2842 https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/article/dbc206886c77407899872ff4d501edb9 kostenfrei https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/toc/1574-7891 Journal toc kostenfrei https://doaj.org/toc/1878-0261 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2022 15 2823-2842 |
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10.1002/1878-0261.13274 doi (DE-627)DOAJ026387085 (DE-599)DOAJdbc206886c77407899872ff4d501edb9 DE-627 ger DE-627 rakwb eng RC254-282 Kamil Mieczkowski verfasserin aut FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. ER FGFR2 JunB luminal breast cancer PR steroid hormones Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Marcin Braun verfasserin aut Barbara Galikowska‐Bogut verfasserin aut Monika Gorska‐Arcisz verfasserin aut Dominika Piasecka verfasserin aut Konrad Stawiski verfasserin aut Anna J. Zaczek verfasserin aut Dariusz Nejc verfasserin aut Radzisław Kordek verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Molecular Oncology Wiley, 2017 16(2022), 15, Seite 2823-2842 (DE-627)531199800 (DE-600)2322586-5 18780261 nnns volume:16 year:2022 number:15 pages:2823-2842 https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/article/dbc206886c77407899872ff4d501edb9 kostenfrei https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/toc/1574-7891 Journal toc kostenfrei https://doaj.org/toc/1878-0261 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2022 15 2823-2842 |
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10.1002/1878-0261.13274 doi (DE-627)DOAJ026387085 (DE-599)DOAJdbc206886c77407899872ff4d501edb9 DE-627 ger DE-627 rakwb eng RC254-282 Kamil Mieczkowski verfasserin aut FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. ER FGFR2 JunB luminal breast cancer PR steroid hormones Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Marcin Braun verfasserin aut Barbara Galikowska‐Bogut verfasserin aut Monika Gorska‐Arcisz verfasserin aut Dominika Piasecka verfasserin aut Konrad Stawiski verfasserin aut Anna J. Zaczek verfasserin aut Dariusz Nejc verfasserin aut Radzisław Kordek verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Molecular Oncology Wiley, 2017 16(2022), 15, Seite 2823-2842 (DE-627)531199800 (DE-600)2322586-5 18780261 nnns volume:16 year:2022 number:15 pages:2823-2842 https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/article/dbc206886c77407899872ff4d501edb9 kostenfrei https://doi.org/10.1002/1878-0261.13274 kostenfrei https://doaj.org/toc/1574-7891 Journal toc kostenfrei https://doaj.org/toc/1878-0261 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2022 15 2823-2842 |
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Kamil Mieczkowski @@aut@@ Kamila Kitowska @@aut@@ Marcin Braun @@aut@@ Barbara Galikowska‐Bogut @@aut@@ Monika Gorska‐Arcisz @@aut@@ Dominika Piasecka @@aut@@ Konrad Stawiski @@aut@@ Anna J. Zaczek @@aut@@ Dariusz Nejc @@aut@@ Radzisław Kordek @@aut@@ Hanna M. Romanska @@aut@@ Rafal Sadej @@aut@@ |
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R - Medicine |
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Kamil Mieczkowski |
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Kamil Mieczkowski misc RC254-282 misc ER misc FGFR2 misc JunB misc luminal breast cancer misc PR misc steroid hormones misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer |
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RC254-282 FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer ER FGFR2 JunB luminal breast cancer PR steroid hormones |
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misc RC254-282 misc ER misc FGFR2 misc JunB misc luminal breast cancer misc PR misc steroid hormones misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
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misc RC254-282 misc ER misc FGFR2 misc JunB misc luminal breast cancer misc PR misc steroid hormones misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
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FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer |
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Kamil Mieczkowski Kamila Kitowska Marcin Braun Barbara Galikowska‐Bogut Monika Gorska‐Arcisz Dominika Piasecka Konrad Stawiski Anna J. Zaczek Dariusz Nejc Radzisław Kordek Hanna M. Romanska Rafal Sadej |
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FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer |
| abstract |
We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. |
| abstractGer |
We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. |
| abstract_unstemmed |
We have recently demonstrated that fibroblast growth factor receptor 2 (FGFR2)‐mediated signalling alters progesterone receptor (PR) activity and response of oestrogen receptor α (ER)‐positive (ER+) breast cancer (BCa) cell lines to anti‐ER agents. Little is known about whether the crosstalk between ER and PR, shown to be modulated by the hormonal background, might also be affected by FGFR2. Here, PR‐dependent behaviour of ER+ BCa cells was studied in the presence of oestrogen (E2) and progesterone (P4) and/or FGF7. In vitro analyses showed that FGF7/FGFR2 signalling: (a) abolished the effect of P4 on E2‐promoted 3D cell growth and response to tamoxifen; (b) regulated ER and PR expression and activity; (c) increased formation of ER–PR complexes; and (d) reversed P4‐triggered deregulation of ER‐dependent genes. Analysis of clinical data demonstrated that the prognostic value of FGFR2 varied between patients with different menopausal status; that is, high expression of FGFR2 was significantly associated with longer progression‐free survival (PFS) in postmenopausal patients, whereas there was no significant association in premenopausal patients. FGFR2 was found to positively correlate with the expression of JunB proto‐oncogene, AP‐1 transcription factor subunit (JUNB), an ER‐dependent gene, only in premenopausal patients. Molecular analyses revealed that the presence of JunB was a prerequisite for FGFR2‐mediated abrogation of P4‐induced inhibition of cell growth. Our results demonstrate for the first time that the FGF7/FGFR2–JunB axis abolishes the modulatory effects of PR on ER‐associated biological functions in premenopausal ER+ BCa. This may provide foundations for a better selection of patients for FGFR‐targeting therapeutic strategies. |
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FGF7/FGFR2–JunB signalling counteracts the effect of progesterone in luminal breast cancer |
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https://doi.org/10.1002/1878-0261.13274 https://doaj.org/article/dbc206886c77407899872ff4d501edb9 https://doaj.org/toc/1574-7891 https://doaj.org/toc/1878-0261 |
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Kamila Kitowska Marcin Braun Barbara Galikowska‐Bogut Monika Gorska‐Arcisz Dominika Piasecka Konrad Stawiski Anna J. Zaczek Dariusz Nejc Radzisław Kordek Hanna M. Romanska Rafal Sadej |
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Kamila Kitowska Marcin Braun Barbara Galikowska‐Bogut Monika Gorska‐Arcisz Dominika Piasecka Konrad Stawiski Anna J. Zaczek Dariusz Nejc Radzisław Kordek Hanna M. Romanska Rafal Sadej |
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2024-07-03T20:41:35.432Z |
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