Journal of Capital Medical University ›› 2019, Vol. 40 ›› Issue (6): 894-900.doi: 10.3969/j.issn.1006-7795.2019.06.016

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Effect of estrogen on the proliferation and nude mouse tumorigenicity of endometrial carcinoma cells by mediating the expression of HOTAIR

Ma Xulan, Xia Di, Wang Huixiao, Jiang Ziwen, Dai Yinmei   

  1. Department of Gynecology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, China
  • Received:2019-07-12 Online:2019-11-21 Published:2019-12-18
  • Supported by:
    This study was supported by Natural Science Foundation of Beijing(7162065).

Abstract: Objective To investigate the effect of estrogen on the proliferation and nude mouse tumorigenicity of endometrial carcinoma cells by mediating the expression of HOTAIR. Methods Lentivirus-mediated interference of HOTAIR expression shHOTAIR and negative control shNC were constructed and transfected into Ishikawa cells, the expression of HOTAIR was detected by qRT-PCR. Four groups were set up:control group (Ishikawa cells), E2 group (E2+Ishikawa cells), E2+shNC group (E2+shNC cells) and E2+shHOTAIR group (E2+shHOTAIR cells). qRT-PCR was used to detect the effect of E2 on the expression of HOTAIR in the four groups. The xenograft tumor model of nude mice treated with E2 and four groups Ishikawa cells of different expression of HOTAIR was constructed. The tumor formation time, the tumor formation rate and the growth curve of the xenograft tumor were recorded. The xenograft tumor was removed, whose volume and weight were measured. The pathological examination of the xenograft tumor was performed. Results The stable transfected cell lines with lentivirus-mediated interference of HOTAIR expression shHOTAIR and negative control shNC were successfully constructed, and the expression of HOTAIR was effectively inhibited (P<0.001). The relative expression of HOTAIR in E2 group was significantly higher than that of control group (P<0.001), and E2+shHOTAIR group was significantly lower than E2+shNC group (P<0.001). The xenograft tumor model of nude mice treated with E2 and four groups Ishikawa cells of different expression of HOTAIR was successfully constructed. The comparison of tumorigenic ability was as follows:E2 group>control group,E2+shNC group>E2+shHOTAIR group. The final volume (P<0.001) and final weight (P<0.001) of the xenograft tumor in E2 group were significantly higher than those in control group, and the final volume (P<0.01) and final weight (P<0.001) in E2+shHOTAIR group were significantly lower than those in E2+shNC group. The HE staining of the xenograft tumor was consistent with the pathological characteristics of endometrial carcinoma cells. Conclusion Estrogen promotes the proliferation and nude mouse tumorigenicity of endometrial carcinoma cells by up-regulating the expression of HOTAIR, which is expected to provide a new target for the treatment of endometrial carcinoma.

Key words: endometrial carcinoma, estrogen, HOTAIR, long non-coding RNAs

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