ErbB receptor signaling and therapeutic resistance to aromatase inhibitors

被引:37
作者
Shin, I
Miller, T
Arteaga, CL
机构
[1] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Comprehens Canc Ctr, Dept Med, Nashville, TN USA
[2] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Comprehens Canc Ctr, Dept Canc Biol, Nashville, TN USA
[3] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Comprehens Canc Ctr, Breast Canc Program, Nashville, TN USA
[4] Hanyang Univ, Dept Life Sci, Seoul 133791, South Korea
关键词
D O I
10.1158/1078-0432.CCR-05-2352
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:1008S / 1012S
页数:5
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