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

Oleh:

Chang, Jui-Hung ; Au, Heng-Kien ; Lee, Wei-Chin ; Chi, Ching-Chi ; Ling, Thai-Yen ; Wang, Le-Ming ; Kao, Shu-Huei ; Huang, Yen-Hua ; Tzeng, Chii-Ruey

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 99 no. 05 (Apr. 2013), page 1332-1339.
Topik: ENDOMETRIOSIS; Stemness; OCT4; cell migration; ectopic endometrium; endometriosis

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2013.04 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

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.

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