Estrogen receptor cofactors expression in breast and endometrial human cancer cells

• Published in: Molecular and cellular endocrinology 1999-10, Vol.156 (1), p.85-93
• Main Authors: Thenot, Sandrine, Charpin, Magali, Bonnet, Sandrine, Cavailles, Vincent
• Format: Article
• Language: English
• Subjects: Adaptor Proteins, Signal Transducing; Antiestrogens; Breast; Breast Neoplasms - genetics; Cancer; Endometrial Neoplasms - genetics; Endometrium; Estrogen receptor; Female; Gene Expression Regulation, Neoplastic; Humans; Nuclear Proteins - genetics; Nuclear Receptor Interacting Protein 1; Protein Isoforms - genetics; Receptors, Estrogen - metabolism; RNA, Messenger - genetics; Selective Estrogen Receptor Modulators - metabolism; Transcription cofactor; Transcription Factors - genetics; Transcription, Genetic; Tumor Cells, Cultured
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/S0303-7207(99)00139-2

In order to approach the molecular basis of the tissue-specific agonistic activity of antioestrogens, we have compared, at the mRNA level, the expression of various transcriptional cofactors (activators or repressors) of estrogen receptors in different breast (MCF7, ZR75-1, T47D, MDA-MB231) and endometrial (Ishikawa, RL-95-2 and HEC1A) human cancer cell lines. We showed that for SRC-1, CBP, TIF1α, RIP140, N-CoR, and SMRT, no significant differences in the expression levels were observed between breast and endometrial cells. For TIF1α mRNA, both isoforms were also detected at similar levels in all the cells tested. By contrast, over-expression of AIB1 mRNA was observed in MCF7 cells, but not in other breast or endometrial cells, irrespective of their ER-status. We then used protein-protein interaction assay (far-Western blot) to confirm the increased expression of at least one of the p160 proteins in MCF7 cells. Finally, we demonstrated that RIP140 mRNA is directly induced by estrogens in ER-positive MCF7 breast cancer cell lines but not in Ishikawa endometrial cells. Together these results indicate that some differences exist between breast and endometrial cancer cell lines at the level of estrogen receptor transcription cofactor expression.