Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis
OCT4 is significantly up-regulated in human ectopic endometriotic tissues. The OCT4 expression may contribute to the pathology of ectopic endometrial growth by stimulating the migration of endometrial cells.
Jui-Hung Chang, Ph.D., Heng-Kien Au, M.D., Wei-Chin Lee, M.S., Ching-Chi Chi, M.D., Thai-Yen Ling, Ph.D., Le-Ming Wang, M.D., Shu-Huei Kao, Ph.D., Yen-Hua Huang, Ph.D., Chii-Ruey Tzeng, M.D.
Volume 99, Issue 5, Pages 1332-1339.e5, April 2013
To identify the impact of the pluripotent transcription factor OCT4 in endometrial cell migration and endometriosis.
OCT4 expression and cell migration study.
Research institution and reproductive medical clinic.
Nine normal-endometrium, 3 normal-myometrium, 36 hyperplastic endometrium, and 58 endometriosis patients.
The expression of OCT4 mRNA in normal endometrium, normal myometrium, hyperplastic endometrium, and ectopic endometriotic tissues was analyzed using reverse transcription and quantitative real-time PCR (RT-QPCR). The effect of OCT4 expression on the migration activity of the endometrial cells was examined.
Main Outcome Measure(s):
RT-QPCR, western blotting, and wound-closure and transwell assays.
The expression of OCT4 and NANOG mRNA 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 mRNA in endometriotic tissues was positively correlated with the expression of genes associated with cell migration. Over-expression 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 upregulated 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.
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