TY - JOUR
T1 - Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis
AU - Chang, Jui Hung
AU - Au, Heng Kien
AU - Lee, Wei Chin
AU - Chi, Ching Chi
AU - Ling, Thai Yen
AU - Wang, Le Ming
AU - Kao, Shu Huei
AU - Huang, Yen Hua
AU - Tzeng, Chii Ruey
PY - 2013/4
Y1 - 2013/4
N2 - Objective: To identify the impact of the pluripotent transcription factor OCT4 in endometrial cell migration and endometriosis. Design: The OCT4 expression and cell migration study. Setting: Research institution and reproductive medical clinic. Patient(s): Nine subjects with normal endometrium, 3 subjects with normal myometrium, 36 patients with hyperplastic endometrium, and 58 patients with endometriosis. Intervention(s): 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. Main Outcome Measure(s): Reverse transcription and quantitative real-time PCR, Western blotting, and wound closure and transwell assays. Result(s): 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. Conclusion(s): 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.
AB - Objective: To identify the impact of the pluripotent transcription factor OCT4 in endometrial cell migration and endometriosis. Design: The OCT4 expression and cell migration study. Setting: Research institution and reproductive medical clinic. Patient(s): Nine subjects with normal endometrium, 3 subjects with normal myometrium, 36 patients with hyperplastic endometrium, and 58 patients with endometriosis. Intervention(s): 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. Main Outcome Measure(s): Reverse transcription and quantitative real-time PCR, Western blotting, and wound closure and transwell assays. Result(s): 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. Conclusion(s): 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.
KW - cell migration
KW - ectopic endometrium
KW - endometriosis
KW - OCT4
KW - Stemness
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U2 - 10.1016/j.fertnstert.2012.11.033
DO - 10.1016/j.fertnstert.2012.11.033
M3 - Article
C2 - 23290742
AN - SCOPUS:84875691636
SN - 0015-0282
VL - 99
SP - 1332
EP - 1339
JO - Fertility and Sterility
JF - Fertility and Sterility
IS - 5
ER -