ArticleReproductive biology and endocrinology : RB&E2021
Expression of Talin-1 in endometriosis and its possible role in pathogenesis.
Article in Reproductive biology and endocrinology : RB&E, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- Molecular mechanisms underlying the inhibition of cell migration and invasion in endometriosis: Advances in pharmacological research (Review).Biomedical reports · 2025Review
- Endometriosis and Cytoskeletal Remodeling: The Functional Role of Actin-Binding Proteins.Cells · 2025Review
- Unraveling pathogenesis, biomarkers and potential therapeutic agents for endometriosis associated with disulfidptosis based on bioinformatics analysis, machine learning and experiment validation.Journal of biological engineering · 2024Article
- Role of Cyclins and Cytoskeletal Proteins in Endometriosis: Insights into Pathophysiology.Cancers · 2024Review
- TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Article
- BCKDK regulates breast cancer cell adhesion and tumor metastasis by inhibiting TRIM21 ubiquitinate talin1.Cell death & disease · 2023Article
- CHCHD2 Regulates Mitochondrial Function and Apoptosis of Ectopic Endometrial Stromal Cells in the Pathogenesis of Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundEndometriosis is a disease that involves active cell invasion and migration. Talin-1 can promote cell invasion, migration and adhension in various cancer cells, but its role in endometriosis has not been investigated. This study was to investigate the expression level of Talin-1 in endometriosis and the role of Talin-1 in the proliferation, adhesion, migration, and invasion of human endometrial stromal cells (ESCs).
methodsEctopic and eutopic endometrial tissues were collected from women with endometriosis, and the control endometrial tissues were obtained from patients without endometriosis. The expression level of Talin-1 was detected in each sample using quantitative real-time polymerase chain reaction and immunohistochemistry. The expression of Talin-1 was inhibited using RNA interference in ESCs, and its proliferation, apoptosis, adhesion, migration, and invasion capacity were analyzed. Western blotting was performed to detect the expression of related molecules after the downregulation of Talin-1.
resultsThe results showed that the mRNA and protein expression of Talin-1 were significantly increased in the ectopic endometrium and eutopic endometrial tissues compared with the controls. The knockdown of Talin-1 did not affect the proliferation and apoptosis of ESCs. The results indicated that the downexpression of Talin-1 inhibited the adhesion, invasion, and migration of ESCs. In addition, the expressions of N-cadherin, MMP-2, and integrin β3 were significantly lower after the deregulation of Talin-1, whereas the levels of E-cadherin were significantly increased.
conclusionsThe expression of Talin-1 was increased in the ectopic and eutopic endometrial tissues compared with the control endometrium. The downregulation of Talin-1 inhibited the adhesion, invasion, and migration of ESCs.
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