作者: Shigehira Saji , Naoki Okumura , Hidetaka Eguchi , Shigeru Nakashima , Akio Suzuki
关键词: Cell culture 、 Estrogen receptor 、 Cancer research 、 Transfection 、 Estrogen receptor alpha 、 Estrogen receptor beta 、 MCF-7 、 Biology 、 Cancer cell 、 Mdm2
摘要: Overexpression of the oncoprotein MDM2, a negative feedback regulator p53, is often observed in breast cancer tissue and cell lines, particularly those which express estrogen receptor alpha (ERalpha). In this study, we report novel function i.e., as positive ERalpha. This does not involve p53. MDM2 overexpressing clones derived from line, MCF-7 cells, showed remarkable growth advantage only estradiol supplemented conditions, profile coincided with increased transcriptional activity ERalpha these cells. Though p53 has been reported to be an inhibitor function, protein was more abundant than parental When exogenously expressed p53-null its enhanced by coexpression MDM2. Mammalian two-hybrid assays GST pull-down indicated that could interact These results indicate direct activator suggest such role for ERalpha-positive cancer.