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
Experimental and therapeutic medicine · 2019 · vol. 17(6) , pp. 4457–4464 · doi:10.3892/etm.2019.7522 · PMID:31105783 · W2941305048
article OA: diamond CC0 RETRACTED ⤵ 18 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Overexpression of TGF-β1 increases proliferation, migration, and invasion of endometrial stromal cells by activating the ERK/MAPK pathway.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

The paper investigated whether TGF‑β1 is altered in endometriosis and how it affects endometrial stromal cells (ESCs), comparing eutopic endometrium from controls (n=6) with endometriosis tissues (n=6). It found significantly elevated TGF‑β expression in endometriosis, and in ESCs, TGF‑β overexpression increased proliferation (with upregulation of PCNA and cyclin D1) and enhanced migration and invasion, accompanied by activation of the ERK/MAPK signaling pathway. Pharmacologic inhibition of ERK/MAPK (U0126) reversed the migration and invasion effects of TGF‑β overexpression, supporting ERK/MAPK as the mechanism. A key limitation stated by design is the small sample size and that functional experiments relied on ESCs with TGF‑β overexpression and in vitro assays, which may not fully capture in vivo disease complexity. This paper is centrally about endometriosis — it links TGF‑β1 overexpression in endometriotic tissue to ESC migration and invasion through ERK/MAPK signaling.

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Abstract

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.

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endometriosis

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