J Cancer 2019; 10(7):1616-1621. doi:10.7150/jca.28218 This issue

Research Paper

Estrogen Enhances Endometrial Cancer Cells Proliferation by Upregulation of Prohibitin

Bin Yang1,2*, Ruiying Chen3*, Xiaoyan Liang1, Jiayan Shi1, Xiaomei Wu4,5, Zhenbo Zhang1,2,4,5, Xiong Chen1,2✉

1. Department of Obstetrics and Gynecology, Shanghai First People's Hospital, Baoshan Branch, Shanghai, 201900, China
2. Jiangxi Medical College, Nanchang University, Nanchang, 330000, China
3. Department of Cervical Diseases, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 200040, China
4. Reproductive Medicine, Department of Obstetrics and Gynecology,Shanghai First people's Hospital, Shanghai Jiaotong University, Shanghai, 201600,China
5. Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai Jiaotong University, Shanghai, 201600, China
*Contributed equally

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Yang B, Chen R, Liang X, Shi J, Wu X, Zhang Z, Chen X. Estrogen Enhances Endometrial Cancer Cells Proliferation by Upregulation of Prohibitin. J Cancer 2019; 10(7):1616-1621. doi:10.7150/jca.28218. Available from https://www.jcancer.org/v10p1616.htm

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Estrogen plays an essential role in type I endometrial cancer cell proliferation. Despite great progresses in the etiology has been obtained in the past, however, the molecular mechanisms remain to be fully clarified. Prohibitin has been demonstrated involvement in multiple cancers' development. If it also contributes to estrogen-driven endometrial cancer proliferation is not clear. IHC assay result display that prohibitin overexpressed in endometrial cancer tissue and associated with the poor prognosis; Western blot assay detect that upregulated prohibitin expression with dose- and time-dependent manners. The cellular growth was monitored with SRB assay which demonstrate that knockdown prohibitin attenuated estrogen-induced proliferation. Ubiquitination assay finds estrogen increased prohibitin level through stabilizing prohibitin protein via inhibition of ubiquitination, while estrogen-induced protein expression was mediated by estrogen receptor. Our findings provide a new insight on the mechanism of estrogen-induced proliferation, implying the possibility of using prohibitin as a potential therapeutic target for the treatment of endometrial cancer.

Keywords: prohibitin, type 1 endometrial cancer, proliferation, estrogen, estrogen receptor