FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells

Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest eff...
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Autor*in:	Lukasz Turczyk [verfasserIn] Kamila Kitowska [verfasserIn] Magdalena Mieszkowska [verfasserIn] Kamil Mieczkowski [verfasserIn] Dominika Czaplinska [verfasserIn] Dominika Piasecka [verfasserIn] Radzisław Kordek [verfasserIn] Andrzej C. Skladanowski [verfasserIn] Piotr Potemski [verfasserIn] Hanna M. Romanska [verfasserIn] Rafal Sadej [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Übergeordnetes Werk:	In: Neoplasia: An International Journal for Oncology Research - Elsevier, 2008, 19(2017), 10, Seite 791-804
Übergeordnetes Werk:	volume:19 ; year:2017 ; number:10 ; pages:791-804

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1016/j.neo.2017.07.006

Katalog-ID:	DOAJ042340969

Internformat


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700	0		\|a Radzisław Kordek \|e verfasserin \|4 aut
700	0		\|a Andrzej C. Skladanowski \|e verfasserin \|4 aut
700	0		\|a Piotr Potemski \|e verfasserin \|4 aut
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700	0		\|a Rafal Sadej \|e verfasserin \|4 aut
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publishDate	2017
allfields	10.1016/j.neo.2017.07.006 doi (DE-627)DOAJ042340969 (DE-599)DOAJ04db79cc2c114e309fb37294afc6a5e9 DE-627 ger DE-627 rakwb eng RC254-282 Lukasz Turczyk verfasserin aut FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Magdalena Mieszkowska verfasserin aut Kamil Mieczkowski verfasserin aut Dominika Czaplinska verfasserin aut Dominika Piasecka verfasserin aut Radzisław Kordek verfasserin aut Andrzej C. Skladanowski verfasserin aut Piotr Potemski verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 19(2017), 10, Seite 791-804 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:19 year:2017 number:10 pages:791-804 https://doi.org/10.1016/j.neo.2017.07.006 kostenfrei https://doaj.org/article/04db79cc2c114e309fb37294afc6a5e9 kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558617301756 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 10 791-804
spelling	10.1016/j.neo.2017.07.006 doi (DE-627)DOAJ042340969 (DE-599)DOAJ04db79cc2c114e309fb37294afc6a5e9 DE-627 ger DE-627 rakwb eng RC254-282 Lukasz Turczyk verfasserin aut FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Magdalena Mieszkowska verfasserin aut Kamil Mieczkowski verfasserin aut Dominika Czaplinska verfasserin aut Dominika Piasecka verfasserin aut Radzisław Kordek verfasserin aut Andrzej C. Skladanowski verfasserin aut Piotr Potemski verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 19(2017), 10, Seite 791-804 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:19 year:2017 number:10 pages:791-804 https://doi.org/10.1016/j.neo.2017.07.006 kostenfrei https://doaj.org/article/04db79cc2c114e309fb37294afc6a5e9 kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558617301756 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 10 791-804
allfields_unstemmed	10.1016/j.neo.2017.07.006 doi (DE-627)DOAJ042340969 (DE-599)DOAJ04db79cc2c114e309fb37294afc6a5e9 DE-627 ger DE-627 rakwb eng RC254-282 Lukasz Turczyk verfasserin aut FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Magdalena Mieszkowska verfasserin aut Kamil Mieczkowski verfasserin aut Dominika Czaplinska verfasserin aut Dominika Piasecka verfasserin aut Radzisław Kordek verfasserin aut Andrzej C. Skladanowski verfasserin aut Piotr Potemski verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 19(2017), 10, Seite 791-804 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:19 year:2017 number:10 pages:791-804 https://doi.org/10.1016/j.neo.2017.07.006 kostenfrei https://doaj.org/article/04db79cc2c114e309fb37294afc6a5e9 kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558617301756 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 10 791-804
allfieldsGer	10.1016/j.neo.2017.07.006 doi (DE-627)DOAJ042340969 (DE-599)DOAJ04db79cc2c114e309fb37294afc6a5e9 DE-627 ger DE-627 rakwb eng RC254-282 Lukasz Turczyk verfasserin aut FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Magdalena Mieszkowska verfasserin aut Kamil Mieczkowski verfasserin aut Dominika Czaplinska verfasserin aut Dominika Piasecka verfasserin aut Radzisław Kordek verfasserin aut Andrzej C. Skladanowski verfasserin aut Piotr Potemski verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 19(2017), 10, Seite 791-804 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:19 year:2017 number:10 pages:791-804 https://doi.org/10.1016/j.neo.2017.07.006 kostenfrei https://doaj.org/article/04db79cc2c114e309fb37294afc6a5e9 kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558617301756 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 10 791-804
allfieldsSound	10.1016/j.neo.2017.07.006 doi (DE-627)DOAJ042340969 (DE-599)DOAJ04db79cc2c114e309fb37294afc6a5e9 DE-627 ger DE-627 rakwb eng RC254-282 Lukasz Turczyk verfasserin aut FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Kamila Kitowska verfasserin aut Magdalena Mieszkowska verfasserin aut Kamil Mieczkowski verfasserin aut Dominika Czaplinska verfasserin aut Dominika Piasecka verfasserin aut Radzisław Kordek verfasserin aut Andrzej C. Skladanowski verfasserin aut Piotr Potemski verfasserin aut Hanna M. Romanska verfasserin aut Rafal Sadej verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 19(2017), 10, Seite 791-804 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:19 year:2017 number:10 pages:791-804 https://doi.org/10.1016/j.neo.2017.07.006 kostenfrei https://doaj.org/article/04db79cc2c114e309fb37294afc6a5e9 kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558617301756 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 10 791-804
language	English
source	In Neoplasia: An International Journal for Oncology Research 19(2017), 10, Seite 791-804 volume:19 year:2017 number:10 pages:791-804
sourceStr	In Neoplasia: An International Journal for Oncology Research 19(2017), 10, Seite 791-804 volume:19 year:2017 number:10 pages:791-804
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Neoplasia: An International Journal for Oncology Research
authorswithroles_txt_mv	Lukasz Turczyk @@aut@@ Kamila Kitowska @@aut@@ Magdalena Mieszkowska @@aut@@ Kamil Mieczkowski @@aut@@ Dominika Czaplinska @@aut@@ Dominika Piasecka @@aut@@ Radzisław Kordek @@aut@@ Andrzej C. Skladanowski @@aut@@ Piotr Potemski @@aut@@ Hanna M. Romanska @@aut@@ Rafal Sadej @@aut@@
publishDateDaySort_date	2017-01-01T00:00:00Z
hierarchy_top_id	320468690
id	DOAJ042340969
language_de	englisch
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callnumber-first	R - Medicine
author	Lukasz Turczyk
spellingShingle	Lukasz Turczyk misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells
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topic_title	RC254-282 FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells
topic	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells
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title_full	FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells
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author_browse	Lukasz Turczyk Kamila Kitowska Magdalena Mieszkowska Kamil Mieczkowski Dominika Czaplinska Dominika Piasecka Radzisław Kordek Andrzej C. Skladanowski Piotr Potemski Hanna M. Romanska Rafal Sadej
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title_sort	fgfr2-driven signaling counteracts tamoxifen effect on erα-positive breast cancer cells
callnumber	RC254-282
title_auth	FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells
abstract	Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy.
abstractGer	Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy.
abstract_unstemmed	Signaling mediated by growth factors receptors has long been suggested as one of the key factors responsible for failure of endocrine treatment in breast cancer (BCa). Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. These results unveil the complexity of ER regulation by FGFR2-mediated signaling likely to be associated with BCa resistance to endocrine therapy.
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title_short	FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells
url	https://doi.org/10.1016/j.neo.2017.07.006 https://doaj.org/article/04db79cc2c114e309fb37294afc6a5e9 http://www.sciencedirect.com/science/article/pii/S1476558617301756 https://doaj.org/toc/1476-5586 https://doaj.org/toc/1522-8002
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Herein we present that in the presence of tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell growth with the strongest effect being produced by FGF7. FGFR2 was identified as a mediator of FGF7 action and the FGFR2-induced signaling was found to underlie cancer-associated fibroblasts-dependent resistance to tamoxifen. FGF7/FGFR2-triggered pathway was shown to induce ER phosphorylation, ubiquitination and subsequent ER proteasomal degradation which counteracted tamoxifen-promoted ER stabilization. We also identified activation of PI3K/AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2-promoted resistance to tamoxifen. Analysis of tissue samples from patients with invasive ductal carcinoma revealed an inversed correlation between expression of FGFR2 and ER, thus supporting our in vitro data. 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FGFR2-Driven Signaling Counteracts Tamoxifen Effect on ERα-Positive Breast Cancer Cells

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