Oral Presentation

Effects of 17β-estradiol on endometrial cancer cell proliferation and HOTAIR expression

Huixiao Wang (CN), Ziwen Jiang (CN), Yinmei Dai (CN)

[Wang] Obstetrics and Gynecology, [Jiang] Obstetrics and Gynecology, [Dai] Obstetrics and Gynecology

Context: Endometrial cancer is the fourth most commonly diagnosed cancer among women, and the role of estrogen in the maintenance and development of endometrial cancer is well established.HOTAIR is the first-found antisense transcription long chain non coding RNA, which has been found to be highly expressed in many kinds of malignant cancers. Objective: To investigate the role of 17β-estradiol in regulating HOTAIR gene expression and cell proliferation in Ishikawa cells. Patients:None Interventions:Endometrial cancer Ishikawa cells were divided into three groups: estradiol (E2) group, HOTAIR-siRNA+E2 group and control group. Main Outcome Measures: We measured the expression of HOTAIR ,the expression of PRC2,and the cell proliferation ability. Methods: Ishikawa cells were hormone-starved then treated or not with 17β-estradiol.HOTAIR expression was measured by qPCR,The role of HOTAIR in cell proliferation was measured following HOTAIR silencing using siRNA.The expression of PRC2(polycomb repressive complex 2), a histone H3 lysine27 (H3K27) specific methyl-transferase complex that interacts with HOTAIR ,was measured by immunoblot analyses. Result:17β-estradio significantly induced cell proliferation in Ishikawa cells. Accordingly, 17β-estradiol significantly increased HOTAIR mRNA expression in Ishikawa cells compared to untreated cells.17β-estradiol increased PRC2 expression .The siRNA silencing of HOTAIR blocked 17β-estradiol-induced cell proliferation and PRC2 expression. Conclusion: This study illustrates that estrogen induces HOTAIR expression in endometrial carcinoma cells. These results support HOTAIR as a therapeutic target in endometrial cancer.