Background: It has been proposed that 17-β- estradiol (E2) activates estrogen receptor and inhibits renal cell carcinoma (RCC) growth. In the present study we explored the role of E2 and ER in the regulation of RCC growth. Materials and Methods: The RCC cell line ACHN was treated by E2 combining with E2 antagonist Fulvestrant or ER knockdown, and cell growth was monitored. Quantitative phosphoproteomics was applied to study the E2 regulated non-genomic phosphorylation changes. Western blotting, immunofluorescence microscopy, and apoptosis assays were used for validation. Results: E2 induced ERdependent growth inhibition in RCC cell lines. Quantitative phosphoproteomics revealed that E2 induced both apoptosis and autophagy. Cellular apoptosis was confirmed by altered.
|頁（從 - 到）||219-230|
|期刊||Cancer Genomics and Proteomics|
|出版狀態||已發佈 - 五月 1 2016|
ASJC Scopus subject areas
- Molecular Biology
- Cancer Research
Chen, K. C., Lin, C. M., Huang, C. J., Chen, S. K., Wu, S. T., Chiang, H-S., & Ku, W. C. (2016). Dual roles of 17-β estradiol in estrogen receptor-dependent growth inhibition in renal cell carcinoma. Cancer Genomics and Proteomics, 13(3), 219-230.