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Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway
Endometriosis is a common gynecological disease with manifestations of endometrial-like tissue outside the uterus. Transforming growth factor-β (TGF-β) is known to facilitate a series of biological events in many cells, including migration. However, the roles of TGF-β in endometriosis still remain l...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6509355/ https://www.ncbi.nlm.nih.gov/pubmed/31105783 http://dx.doi.org/10.3892/etm.2019.7522 |
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author | Liu, Zhihong Yi, Lisha Du, Miaomiao Gong, Guifang Zhu, Yali |
author_facet | Liu, Zhihong Yi, Lisha Du, Miaomiao Gong, Guifang Zhu, Yali |
author_sort | Liu, Zhihong |
collection | PubMed |
description | Endometriosis is a common gynecological disease with manifestations of endometrial-like tissue outside the uterus. Transforming growth factor-β (TGF-β) is known to facilitate a series of biological events in many cells, including migration. However, the roles of TGF-β in endometriosis still remain largely unknown. The aim of the present study was to discover the role of TGF-β1 in endometriosis development and progression and its associated mechanisms. It was demonstrated that the expression of TGF-β1 was significantly elevated in endometriosis in comparison with that in normal tissue. Overexpression of TGF-β increased the proliferation and upregulated proliferating cell nuclear antigen and cyclin D1 in endometrial stromal cells (ESCs). Furthermore, TGF-β overexpression also triggered a series of biological events occurring in ESCs, including cell migration and invasion, and activated the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling pathway. The inhibition of the ERK/MAPK pathway reversed the previous effects of TGF-β overexpression. Collectively, the present results indicate that overexpression of TGF-β enhances the migration and invasion of ectopic ESCs via the ERK/MAPK signaling pathway, providing theoretical evidence for the development of new treatment methods targeting the TGF-β-ERK/MAPK signaling pathway for prophylaxis of endometriosis. |
format | Online Article Text |
id | pubmed-6509355 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65093552019-05-18 Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway Liu, Zhihong Yi, Lisha Du, Miaomiao Gong, Guifang Zhu, Yali Exp Ther Med Articles Endometriosis is a common gynecological disease with manifestations of endometrial-like tissue outside the uterus. Transforming growth factor-β (TGF-β) is known to facilitate a series of biological events in many cells, including migration. However, the roles of TGF-β in endometriosis still remain largely unknown. The aim of the present study was to discover the role of TGF-β1 in endometriosis development and progression and its associated mechanisms. It was demonstrated that the expression of TGF-β1 was significantly elevated in endometriosis in comparison with that in normal tissue. Overexpression of TGF-β increased the proliferation and upregulated proliferating cell nuclear antigen and cyclin D1 in endometrial stromal cells (ESCs). Furthermore, TGF-β overexpression also triggered a series of biological events occurring in ESCs, including cell migration and invasion, and activated the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling pathway. The inhibition of the ERK/MAPK pathway reversed the previous effects of TGF-β overexpression. Collectively, the present results indicate that overexpression of TGF-β enhances the migration and invasion of ectopic ESCs via the ERK/MAPK signaling pathway, providing theoretical evidence for the development of new treatment methods targeting the TGF-β-ERK/MAPK signaling pathway for prophylaxis of endometriosis. D.A. Spandidos 2019-06 2019-04-23 /pmc/articles/PMC6509355/ /pubmed/31105783 http://dx.doi.org/10.3892/etm.2019.7522 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Liu, Zhihong Yi, Lisha Du, Miaomiao Gong, Guifang Zhu, Yali Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway |
title | Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway |
title_full | Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway |
title_fullStr | Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway |
title_full_unstemmed | Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway |
title_short | Overexpression of TGF-β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway |
title_sort | overexpression of tgf-β enhances the migration and invasive ability of ectopic endometrial cells via erk/mapk signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6509355/ https://www.ncbi.nlm.nih.gov/pubmed/31105783 http://dx.doi.org/10.3892/etm.2019.7522 |
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