The functional implications of Akt activity and TGF-beta signaling in tamoxifen-resistant breast cancer
DC Field | Value | Language |
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dc.contributor.author | Yoo, Young A. | - |
dc.contributor.author | Kim, Yeul Hong | - |
dc.contributor.author | Kim, Jun Suk | - |
dc.contributor.author | Seo, Jae Hong | - |
dc.date.accessioned | 2021-09-09T10:55:41Z | - |
dc.date.available | 2021-09-09T10:55:41Z | - |
dc.date.created | 2021-06-10 | - |
dc.date.issued | 2008-03 | - |
dc.identifier.issn | 0167-4889 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/124032 | - |
dc.description.abstract | Development of acquired resistance to tamoxifen is a major clinical problem during endocrine treatment in estrogen receptor positive breast cancer. Transforming growth factor-beta 1 (TGF-beta) has been implicated in tamoxifen-induced cellular signaling in breast cancer, and increased Akt activation is associated with tamoxifen-resistant cell types. We hypothesized that the relationship between TGF-beta and Akt signaling may be involved in the development and progression of tamoxifen resistance. Tamoxifen-resistant (Tam-R) cells were established from parental MCF-7 cells by continuously exposing them to 4-hydroxytamoxifen (4-OHT). Tam-R cells were associated with a decrease in TGF-beta 1 secretion, TGF-beta-mediated transcriptional response, and growth inhibitory effects of 4-OHT. Tam-R cells expressed significantly higher levels of phosphorylated Akt and lower levels of phosphorylated Smad 3 in both the absence and presence of 4-OHT when compared to MCF-7 cells treated with 4-OHT. Ectopic expression of constitutively active Akt (Myc-Akt(Myr)) rendered MCF-7 cells resistant to activation by TGF-beta and the growth inhibitory effects of 4-OHT, while over-expression of kinase-dead Akt (Myc-Akt(K179M)) or LY294002 treatment of Tam-R cells enhanced TGF-beta activation and blocked cell growth. These results suggest that suppression of TGF+ signaling by activated Akt is correlated with the development of tamoxifen resistance in breast cancer. (c) 2007 Elsevier B.V. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCIENCE BV | - |
dc.subject | GROWTH-FACTOR-BETA | - |
dc.subject | PROTEIN-KINASE B/AKT | - |
dc.subject | MCF-7 CELLS | - |
dc.subject | ANTIESTROGENS INDUCE | - |
dc.subject | EPITHELIAL-CELLS | - |
dc.subject | SMAD PATHWAY | - |
dc.subject | RECEPTOR | - |
dc.subject | MECHANISMS | - |
dc.subject | ACTIVATION | - |
dc.subject | APOPTOSIS | - |
dc.title | The functional implications of Akt activity and TGF-beta signaling in tamoxifen-resistant breast cancer | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Yoo, Young A. | - |
dc.contributor.affiliatedAuthor | Kim, Yeul Hong | - |
dc.contributor.affiliatedAuthor | Kim, Jun Suk | - |
dc.contributor.affiliatedAuthor | Seo, Jae Hong | - |
dc.identifier.doi | 10.1016/j.bbamcr.2007.12.001 | - |
dc.identifier.wosid | 000254185100009 | - |
dc.identifier.bibliographicCitation | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, v.1783, no.3, pp.438 - 447 | - |
dc.relation.isPartOf | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | - |
dc.citation.title | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | - |
dc.citation.volume | 1783 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 438 | - |
dc.citation.endPage | 447 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | GROWTH-FACTOR-BETA | - |
dc.subject.keywordPlus | PROTEIN-KINASE B/AKT | - |
dc.subject.keywordPlus | MCF-7 CELLS | - |
dc.subject.keywordPlus | ANTIESTROGENS INDUCE | - |
dc.subject.keywordPlus | EPITHELIAL-CELLS | - |
dc.subject.keywordPlus | SMAD PATHWAY | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordAuthor | tamoxifen | - |
dc.subject.keywordAuthor | Akt | - |
dc.subject.keywordAuthor | transforming growth factor-beta | - |
dc.subject.keywordAuthor | breast cancer | - |
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