Overexpression of TGF‑β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway
- Zhihong Liu
- Lisha Yi
- Miaomiao Du
- Guifang Gong
- Yali Zhu
Affiliations: Department of Obstetrics and Gynecology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510623, P.R. China
- Published online on: April 23, 2019 https://doi.org/10.3892/etm.2019.7522
Copyright : © Liu
et al. This is an open access article distributed under the
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Commons Attribution License [CC BY 4.0].
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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.