Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis.

Research paper by Jui-Hung JH Chang, Heng-Kien HK Au, Wei-Chin WC Lee, Ching-Chi CC Chi, Thai-Yen TY Ling, Le-Ming LM Wang, Shu-Huei SH Kao, Yen-Hua YH Huang, Chii-Ruey CR Tzeng

Indexed on: 08 Jan '13Published on: 08 Jan '13Published in: Fertility and Sterility®


To identify the impact of the pluripotent transcription factor OCT4 in endometrial cell migration and endometriosis.The OCT4 expression and cell migration study.Research institution and reproductive medical clinic.Nine subjects with normal endometrium, 3 subjects with normal myometrium, 36 patients with hyperplastic endometrium, and 58 patients with endometriosis.The expression of OCT4 messenger RNA in normal endometrium, normal myometrium, hyperplastic endometrium, and ectopic endometriotic tissues was analyzed using reverse transcription and quantitative real-time polymerase chain reaction (PCR). The effect of OCT4 expression on the migration activity of the endometrial cells was examined.Reverse transcription and quantitative real-time PCR, Western blotting, and wound closure and transwell assays.The expression of OCT4 and NANOG messenger RNA was significantly higher in ectopic endometriotic tissues, compared with that of the normal endometrium, the normal myometrium, and the hyperplastic endometrium. The level of OCT4 messenger RNA in endometriotic tissues was positively correlated with the expression of genes associated with cell migration. Overexpression of the OCT4 protein in primary human endometriotic stromal cells and human RL95-2 and HEC1A endometrial carcinoma cell lines resulted in decreased levels of E-CADHERIN, the increased expression of the VIMENTIN, TWIST, and SLUG proteins, and an increase in the migration activity of endometrial cells in transwell and wound closure assays.The transcription of the OCT4 gene is significantly up-regulated in human ectopic endometriotic tissues. The expression of OCT4 may contribute to the pathology of ectopic endometrial growth by stimulating the migration activity of endometrial cells.