Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway

Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promote...
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Gespeichert in:

Autor*in:	Zhaojia Wu [verfasserIn] Tong Niu [verfasserIn] Wei Xiao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance

Übergeordnetes Werk:	In: Cancer Cell International - BMC, 2003, 19(2019), 1, Seite 15
Übergeordnetes Werk:	volume:19 ; year:2019 ; number:1 ; pages:15

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s12935-019-1050-4

Katalog-ID:	DOAJ061989525

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520			\|a Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.
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allfields	10.1186/s12935-019-1050-4 doi (DE-627)DOAJ061989525 (DE-599)DOAJ3c7f6c4baa2c412e8109e9fd16886c64 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Zhaojia Wu verfasserin aut Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers. Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Tong Niu verfasserin aut Wei Xiao verfasserin aut In Cancer Cell International BMC, 2003 19(2019), 1, Seite 15 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:19 year:2019 number:1 pages:15 https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/article/3c7f6c4baa2c412e8109e9fd16886c64 kostenfrei https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2019 1 15
spelling	10.1186/s12935-019-1050-4 doi (DE-627)DOAJ061989525 (DE-599)DOAJ3c7f6c4baa2c412e8109e9fd16886c64 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Zhaojia Wu verfasserin aut Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers. Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Tong Niu verfasserin aut Wei Xiao verfasserin aut In Cancer Cell International BMC, 2003 19(2019), 1, Seite 15 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:19 year:2019 number:1 pages:15 https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/article/3c7f6c4baa2c412e8109e9fd16886c64 kostenfrei https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2019 1 15
allfields_unstemmed	10.1186/s12935-019-1050-4 doi (DE-627)DOAJ061989525 (DE-599)DOAJ3c7f6c4baa2c412e8109e9fd16886c64 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Zhaojia Wu verfasserin aut Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers. Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Tong Niu verfasserin aut Wei Xiao verfasserin aut In Cancer Cell International BMC, 2003 19(2019), 1, Seite 15 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:19 year:2019 number:1 pages:15 https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/article/3c7f6c4baa2c412e8109e9fd16886c64 kostenfrei https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2019 1 15
allfieldsGer	10.1186/s12935-019-1050-4 doi (DE-627)DOAJ061989525 (DE-599)DOAJ3c7f6c4baa2c412e8109e9fd16886c64 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Zhaojia Wu verfasserin aut Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers. Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Tong Niu verfasserin aut Wei Xiao verfasserin aut In Cancer Cell International BMC, 2003 19(2019), 1, Seite 15 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:19 year:2019 number:1 pages:15 https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/article/3c7f6c4baa2c412e8109e9fd16886c64 kostenfrei https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2019 1 15
allfieldsSound	10.1186/s12935-019-1050-4 doi (DE-627)DOAJ061989525 (DE-599)DOAJ3c7f6c4baa2c412e8109e9fd16886c64 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Zhaojia Wu verfasserin aut Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers. Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Tong Niu verfasserin aut Wei Xiao verfasserin aut In Cancer Cell International BMC, 2003 19(2019), 1, Seite 15 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:19 year:2019 number:1 pages:15 https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/article/3c7f6c4baa2c412e8109e9fd16886c64 kostenfrei https://doi.org/10.1186/s12935-019-1050-4 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2019 1 15
language	English
source	In Cancer Cell International 19(2019), 1, Seite 15 volume:19 year:2019 number:1 pages:15
sourceStr	In Cancer Cell International 19(2019), 1, Seite 15 volume:19 year:2019 number:1 pages:15
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topic_facet	Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology
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container_title	Cancer Cell International
authorswithroles_txt_mv	Zhaojia Wu @@aut@@ Tong Niu @@aut@@ Wei Xiao @@aut@@
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Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Uev1A</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">AKT/FOXO1/BIM pathway</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cell survival</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chemoresistance</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. 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callnumber-first	R - Medicine
author	Zhaojia Wu
spellingShingle	Zhaojia Wu misc RC254-282 misc QH573-671 misc Uev1A misc AKT/FOXO1/BIM pathway misc Cell survival misc Chemoresistance misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens misc Cytology Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway
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topic_title	RC254-282 QH573-671 Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway Uev1A AKT/FOXO1/BIM pathway Cell survival Chemoresistance
topic	misc RC254-282 misc QH573-671 misc Uev1A misc AKT/FOXO1/BIM pathway misc Cell survival misc Chemoresistance misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens misc Cytology
topic_unstemmed	misc RC254-282 misc QH573-671 misc Uev1A misc AKT/FOXO1/BIM pathway misc Cell survival misc Chemoresistance misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens misc Cytology
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title	Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway
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title_full	Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway
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title_sort	uev1a promotes breast cancer cell survival and chemoresistance through the akt-foxo1-bim pathway
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title_auth	Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway
abstract	Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.
abstractGer	Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.
abstract_unstemmed	Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.
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title_short	Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway
url	https://doi.org/10.1186/s12935-019-1050-4 https://doaj.org/article/3c7f6c4baa2c412e8109e9fd16886c64 https://doaj.org/toc/1475-2867
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up_date	2024-07-03T23:45:36.631Z
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Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Uev1A</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">AKT/FOXO1/BIM pathway</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cell survival</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chemoresistance</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. 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Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway

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