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dc.contributor.author신인철-
dc.date.accessioned2022-12-05T00:36:46Z-
dc.date.available2022-12-05T00:36:46Z-
dc.date.issued2021-06-
dc.identifier.citationJournal of Cell Science, v. 134, NO. 11, article no. jcs256503, Page. 1-18en_US
dc.identifier.issn0021-9533;1477-9137en_US
dc.identifier.urihttps://journals.biologists.com/jcs/article/134/11/jcs256503/269035/YAP-CTGF-and-Cyr61-are-overexpressed-in-tamoxifenen_US
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/177887-
dc.description.abstractAbout 70% of breast cancers overexpress estrogen receptor α (ERα, encoded by ESR1). Tamoxifen, a competitive inhibitor of estrogen that binds to ER, has been widely used as a treatment for ER-positive breast cancer. However, 20–30% of breast cancer is resistant to tamoxifen treatment. The mechanisms underlying tamoxifen resistance remain elusive. We found that Yes-associated protein (YAP; also known as YAP1), connective tissue growth factor (CTGF; also known as CCN2) and cysteine-rich angiogenic inducer 61 (Cyr61; also known as CCN1) are overexpressed, while ERα is downregulated in tamoxifen-resistant breast cancer. Inhibition of YAP, CTGF and Cyr61 restored ERα expression and increased sensitivity to tamoxifen. Overexpression of YAP, CTGF, and Cyr61 led to downregulation of ERα and conferred resistance to tamoxifen in ER-positive breast cancer cells. Mechanistically, CTGF and Cyr61 downregulated ERα expression at the transcriptional level by directly binding to the regulatory regions of the ERα-encoding gene, leading to increased tamoxifen resistance. Also, CTGF induced Glut3 (also known as SLC2A3) expression, leading to increased glycolysis, which enhanced cell proliferation and migration in tamoxifen-resistant cells. Together, these results demonstrate a novel role of YAP, CTGF and Cyr61 in tamoxifen resistance and provide a molecular basis for their function in tamoxifen-resistant breast cancer. © 2021. Published by The Company of Biologists Ltden_US
dc.description.sponsorshipThis work was supported by National Research Foundation of Korea (NRF) grants funded by the Korea government (MIST) (2019R1H1A2079999, 2020R1F1A1048616, 2020R1A6A3A13074546).en_US
dc.languageenen_US
dc.publisherCompany of Biologists Ltden_US
dc.subjectTamoxifen resistanceen_US
dc.subjectBreast canceren_US
dc.subjectEstrogen receptoren_US
dc.subjectCTGFen_US
dc.subjectCyr61en_US
dc.titleYAP, CTGF and Cyr61 are overexpressed in tamoxifen-resistant breast cancer and induce transcriptional repression of ERαen_US
dc.typeArticleen_US
dc.relation.no11-
dc.relation.volume134-
dc.identifier.doi10.1242/jcs.256503en_US
dc.relation.page1-18-
dc.relation.journalJournal of Cell Science-
dc.contributor.googleauthorKim, Hyungjoo-
dc.contributor.googleauthorSon, Seogho-
dc.contributor.googleauthorKo, Yunhyo-
dc.contributor.googleauthorLee, Jeong Eon-
dc.contributor.googleauthorShin, Incheol-
dc.contributor.googleauthorKim, Sangmin-
dc.sector.campusS-
dc.sector.daehak자연과학대학-
dc.sector.department생명과학과-
dc.identifier.pidincheol-
dc.identifier.orcidhttps://orcid.org/0000-0003-3172-2594-
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COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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