Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이경은 | * |
dc.contributor.author | 남은미 | * |
dc.date.accessioned | 2016-08-28T11:08:47Z | - |
dc.date.available | 2016-08-28T11:08:47Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 1932-6203 | * |
dc.identifier.other | OAK-18788 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218276 | - |
dc.description.abstract | Background The beta-catenin signaling is important in cell growth and differentiation and is frequently dys-regulated in various cancers. The most well-known mechanism of endocrine resistance is cross-talk between the estrogen receptor (ER) and other growth factor signaling, such as phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) signaling pathway. In the present study, we investigated whether beta-catenin could be a potential target to overcome endocrine resistance in breast cancer. Methods We established tamoxifen-resistant (TamR) cell line via long-term exposure of MCF-7 breast cancer cells to gradually increasing concentrations of tamoxifen. The levels of protein expression and mRNA transcripts were determined using western blot analysis and real-time quantitative PCR. The transcriptional activity of beta-catenin was measured using luciferase activity assay. Results TamR cells showed a mesenchymal phenotype, and exhibited a relatively decreased expression of ER and increased expression of human epidermal growth factor receptor 2 and the epidermal growth factor receptor. We confirmed that the expression and transcriptional activity of beta-catenin were increased in TamR cells compared with control cells. The expression and transcriptional activity of beta-catenin were inhibited by beta-catenin small-molecule inhibitor, ICG-001 or beta-catenin siRNA. The viability of TamR cells, which showed no change after treatment with tamoxifen, was reduced by ICG-001 or beta-catenin siRNA. The combination of ICG-001 and mTOR inhibitor, rapamycin, yielded an additive effect on the inhibition of viability in TamR cells. Conclusion These results suggest that beta-catenin plays a role in tamoxifen-resistant breast cancer, and the inhibition of beta-catenin may be a potential target in tamoxifen-resistant breast cancer. | * |
dc.language | English | * |
dc.publisher | PUBLIC LIBRARY SCIENCE | * |
dc.title | Inhibition of beta-Catenin to Overcome Endocrine Resistance in Tamoxifen-Resistant Breast Cancer Cell Line | * |
dc.type | Article | * |
dc.relation.issue | 5 | * |
dc.relation.volume | 11 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | PLOS ONE | * |
dc.identifier.doi | 10.1371/journal.pone.0155983 | * |
dc.identifier.wosid | WOS:000376291100144 | * |
dc.identifier.scopusid | 2-s2.0-84971272995 | * |
dc.author.google | Won, Hye Sung | * |
dc.author.google | Lee, Kyung Mee | * |
dc.author.google | Oh, Ju Eon | * |
dc.author.google | Nam, Eun Mi | * |
dc.author.google | Lee, Kyoung Eun | * |
dc.contributor.scopusid | 이경은(7501517217;58364338700) | * |
dc.contributor.scopusid | 남은미(7005824288;57226666155) | * |
dc.date.modifydate | 20240301081003 | * |