Knockdown of vascular cell adhesion molecule 1 impedes transforming growth factor beta 1-mediated proliferation, migration, and invasion of endometriotic cyst stromal cells

Juan Zhang, Hui Li, Dan Yi, Chuntian Lai, Haiyan Wang, Wenda Zou, Bei Cao
Reproductive biology and endocrinology : RB&E · 2019 · vol. 17(1) , pp. 69 · doi:10.1186/s12958-019-0512-9 · PMID:31443713 · PMC6708153 · W2969505387
article OA: gold CC0 ⤵ 17 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that vascular cell adhesion molecule 1 (VCAM-1) knockdown impedes transforming growth factor beta 1 (TGF-β1)-mediated proliferation, migration, and invasion of endometriotic cyst stromal cells.

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

This study examined how transforming growth factor beta 1 (TGF-β1) regulates vascular cell adhesion molecule 1 (VCAM-1) and affects proliferation, migration, and invasion in human endometriotic cyst stromal cells. Endometriotic and normal endometrial tissues from 17 patients each were analyzed by qRT-PCR and western blotting, and cultured cells were treated with recombinant TGF-β1 and subjected to siRNA knockdown of TGF-β1, VCAM-1, or Smad3, with functional readouts using CCK-8, EdU assays, and transwell migration/invasion assays. The authors found that TGF-β1 and VCAM-1 were upregulated in endometriotic tissues, that TGF-β1 increased VCAM-1 protein via Smad3, and that silencing VCAM-1 blocked TGF-β1-driven proliferation, migration, and invasion. The key limitation explicitly stated in the methods/results is the in vitro nature of functional testing in endometriotic cyst stromal cells rather than in vivo validation, though tissue expression was measured in patients; overall, this paper supports a mechanism linking VCAM-1 to TGF-β1 signaling outcomes in endometriosis. This paper is centrally about endometriosis — it investigates VCAM-1’s role in TGF-β1-mediated proliferation, migration, and invasion of endometriotic cyst stromal cells.

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Abstract

PURPOSE: Endometriosis is one of the most common, difficult, and complicated gynecological disorders. Vascular cell adhesion molecule 1 (VCAM-1) has been reported to be aberrantly expressed in patients with endometriosis. However, the exact role and mechanism of VCAM-1 in endometriosis remains unclear. METHODS: The expression of transforming growth factor beta 1 (TGF-β1) and VCAM-1 was determined by quantitative real-time polymerase chain reaction and western blotting. Human endometriotic cells were cultured and their responsiveness to TGF-β1 was evaluated by Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine, and transwell migration and invasion assays. RESULTS: The levels of TGF-β1 and VCAM-1 mRNA were upregulated in the endometriotic tissues. Knockdown of TGF-β1 in endometriotic cyst stromal cells caused a marked inhibition of cell proliferation, migration, and invasion. Treatment of endometriotic cyst stromal cells with TGF-β1 resulted in an obvious promotion of cell proliferation, migration, and invasion, and strikingly increased the protein expression of VCAM-1. Silencing of Smad3 abated TGF-β1-stimulated VCAM-1 expression. Furthermore, the promoting effects of TGF-β1 on the proliferation, migration, and invasion of endometriotic cyst stromal cells were blocked by silencing of VCAM-1. CONCLUSION: Knockdown of VCAM-1 impedes TGF-β1-mediated proliferation, migration, and invasion of endometrial cells, thereby indicating that VCAM-1 may serve as a therapeutic target for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Cell Movement Cell Proliferation Cysts Endometriosis RNA Interference Stromal Cells Transforming Growth Factor beta Transforming Growth Factor beta1 Adult Cell Movement Cell Movement Cell Proliferation Cell Proliferation Cells, Cultured Cell Survival Cell Survival Cell Survival Cysts Cysts Cysts

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