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

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

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1332-1339
Number of pages8
JournalFertility and Sterility
Volume99
Issue number5
DOIs
Publication statusPublished - Apr 2013

Fingerprint

Endometriosis
Endometrium
Cell Movement
Transcription Factors
Choristoma
Myometrium
Messenger RNA
Reverse Transcription
Real-Time Polymerase Chain Reaction
Wounds and Injuries
Endometrial Neoplasms
Stromal Cells
Proteins
Western Blotting
Outcome Assessment (Health Care)
Pathology
Gene Expression
Cell Line
Growth
Research

Keywords

  • cell migration
  • ectopic endometrium
  • endometriosis
  • OCT4
  • Stemness

ASJC Scopus subject areas

  • Obstetrics and Gynaecology
  • Reproductive Medicine

Cite this

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

In: Fertility and Sterility, Vol. 99, No. 5, 04.2013, p. 1332-1339.

Research output: Contribution to journalArticle

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. / Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis. In: Fertility and Sterility. 2013 ; Vol. 99, No. 5. pp. 1332-1339.
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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

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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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