ErbB receptor signaling and therapeutic resistance to aromatase inhibitors
- Authors
- Shin, In cheol; Miller, Todd; Arteaga, Carlos L.
- Issue Date
- Feb-2006
- Publisher
- AMER ASSOC CANCER RESEARCH
- Citation
- CLINICAL CANCER RESEARCH, v.12, no.3, pp.1008S - 1012S
- Indexed
- SCIE
SCOPUS
- Journal Title
- CLINICAL CANCER RESEARCH
- Volume
- 12
- Number
- 3
- Start Page
- 1008S
- End Page
- 1012S
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/181802
- DOI
- 10.1158/1078-0432.CCR-05-2352
- ISSN
- 1078-0432
- Abstract
- We have investigated the effect of HER-2 overexpression on resistance to the aromatase inhibitor letrozole in MCF-7 breast cancer cells stably expressing cellular aromatase (MCF-7/CA). MCF-7/ CA cells overexpressing HER-2 showed > 2-fold increase in estrogen receptor (ER)-mediated transcriptional reporter activity upon treatment with androstenedione compared with vector-only control MCF-7/CA cells. Cotreatment with letrozole did not abrogate androstenedione-induced transcription and cell proliferation in HER-2-overexpressing cells. Chromatin immunoprecipitation assays using cross-linked protein-DNA from MCF-7/CA/HER-2 cells indicated ligand-independent association of the ER alpha coactivators AIB-1 and CBP to the promoter region of the estrogen-responsive pS2 gene. Upon treatment with androstenedione, there were increased associations of AIB1 and CBP with the pS2 promoter in the HER-2-overexpressing compared with control MCF-7/CA cells. These results suggest that ligand-independent recruitment of coactivator complexes to estrogen-responsive promoters as a result of HER-2 overexpression may play a role in the development of letrozole resistance.
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