TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis

Heng-Kien Au, Jui-Hung Chang, Yu-Chih Wu, Yung‐Che Kuo, Yung-Che Kuo, Yu-Hsi Chen, Wei-Chin Lee, Te-Sheng Chang, Pei‐Chi Lan, Pei-Chi Lan, Hung-Chih Kuo, Kha‐Liang Lee, Kha-Liang Lee, Mei-Tsu Lee, Chii‐Ruey Tzeng, Chii-Ruey Tzeng, Yen-Hua Huang, Yen‐Hua Huang
PloS one · 2015 · vol. 10(12) , pp. e0145256 · doi:10.1371/journal.pone.0145256 · PMID:26675296 · PMC4682958 · W2201327900
article OA: gold CC0 ⤵ 23 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

TGF-βI upregulates OCT4, SNAIL, and N-Cadherin, increasing endometriotic cell migration and contributing to ectopic endometrial growth.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study examined how TGF-βI signaling affects expression of the pluripotent transcription factor OCT4 and regulates migration-related genes in endometriotic tissues. Using microdissected human samples categorized by high vs low migratory capacity (adenomyotic myometrium and chocolate cyst vs normal/hyperplastic endometrium) and in vitro treatments with TGF-βI (including cytokines for comparison), the authors found higher TGF-β receptor I (TGF-β RI) and OCT4 expression in high-migratory ectopic tissues, with positive correlations linking TGF-β RI or OCT4 to migration-associated genes (SNAIL, SLUG, TWIST); TGF-βI also dose-dependently increased OCT4, SNAIL, and N-cadherin and enhanced migration. Silencing OCT4 suppressed TGF-βI-induced N-cadherin/SNAIL expression and reduced migration in primary endometriotic stromal cells and endometrial carcinoma cell lines (RL95-2, HEC1A) by wound-closure and transwell assays, with F-actin redistribution. A limitation is that OCT4 knockdown and migration readouts were validated across cell models rather than tested in vivo, and tissue data are observational with correlations rather than mechanistic proof. This paper is centrally about endometriosis — it identifies TGF-βI/TGF-βRI–OCT4 signaling as a mechanism driving endometriotic cell migration, with specific experiments using adenomyotic and endometriosis-derived tissues and cells.

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Abstract

Transforming growth factor (TGF-β)/TGF-β receptor signal is known to promote cell migration. Up-regulation of TGF-β in serum/peritoneal fluid and increased levels of pluripotent transcription factor OCT4 in endometriotic tissues are frequently observed in patients with endometriosis. However, the mechanisms underlying how TGF-β/TGF-β receptor and OCT4 affect endometriotic cell migration still remain largely unknown. Therefore, endometriotic tissue with high cell migratory capacity were collected from patients with adenomyotic myometrium (n = 23) and chocolate cyst (n = 24); and endometrial tissue with low cell migratory capacity in normal endometrium or hyperplastic endometrium (n = 8) were collected as the controls. We found the mRNA levels of TGF-β receptor I (TGF-β RI) and OCT4 were significantly higher in the high-migratory ectopic endometriotic tissues than those of the low-migratory normal or hyperplastic endometrium. Positive correlations between TGF-β RI and OCT4, and either TGF-β RI or OCT4 with migration-related genes (SNAIL, SLUG and TWIST) regarding the mRNA levels were observed in human endometriotic tissues. TGF-βI dose-dependently increased the gene and protein levels of OCT4, SNAIL and N-Cadherin (N-CAD) and silencing of endogenous OCT4 significantly suppressed the TGF-βI-induced expressions of N-CAD and SNAIL in primary human endometriotic stromal cells and human endometrial carcinoma cell lines RL95-2 and HEC1A. Furthermore, TGF-βI significantly increased the migration ability of endometriotic cells and silencing of OCT4 dramatically suppressed the TGF-βI-induced cell migration activity evidenced by wound-closure assay, transwell assay, and confocal image of F-actin cellular distribution. In conclusion, the present findings demonstrate that the niche TGF-β plays a critical role in initiating expressions of pluripotent transcription factor OCT4 which may contribute to the ectopic endometrial growth by stimulating endometrial cell migration. These findings would be useful for developing therapeutic strategies targeting TGF-β-OCT4 signaling to prevent endometriosis in the future.

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Condition tags

endometriosis

MeSH descriptors

Cell Movement Endometriosis Octamer Transcription Factor-3 Transforming Growth Factor beta1 Adult Cadherins Cadherins Cadherins Cell Line, Tumor Endometriosis Female Humans Middle Aged Nuclear Proteins Nuclear Proteins Nuclear Proteins Octamer Transcription Factor-3 Octamer Transcription Factor-3 Protein Serine-Threonine Kinases Protein Serine-Threonine Kinases

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