ArticleReproductive sciences (Thousand Oaks, Calif.)2021
Talin1 Induces Epithelial-Mesenchymal Transition to Facilitate Endometrial Cell Migration and Invasion in Adenomyosis Under the Regulation of microRNA-145-5p.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Non-Coding RNAs (microRNAs, lncRNAs, circRNAs) in Adenomyosis: A Systematic Review of Mechanistic and Translational Evidence.International journal of molecular sciences · 2025Pooled it
- MicroRNAs as Biomarkers for Adenomyosis: A Systematic Review.Biomedicines · 2026Review
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Pathogenesis of Adenomyosis: An Integrated Review of Cellular Origins, Molecular Mechanisms, and Intersecting Diseases.Journal of cellular and molecular medicine · 2026Review
- Shared and distinct molecular pathways in eutopic endometrium of endometriosis and adenomyosis patients: a transcriptomic study in Chinese women.BMC women's health · 2025Article
- Talin1 promotes HCC progression by regulating NRG1/PI3K/AKT pathway.Discover oncology · 2024Article
- Review
- Exosomes: potential diagnostic markers and drug carriers for adenomyosis.Frontiers in pharmacology · 2023Review
- Estrogen-increased SGK1 Promotes Endometrial Stromal Cell Invasion in Adenomyosis by Regulating with LPAR2.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Unveiling the Pathogenesis of Adenomyosis through Animal Models.Journal of clinical medicine · 2022Review
- Exploration the global single-cell ecological landscape of adenomyosis-related cell clusters by single-cell RNA sequencing.Frontiers in genetics · 2022Article
- Conservative Management of Uterine Adenomyosis: Medical vs. Surgical Approach.Journal of clinical medicine · 2021Review
- Upregulated Talin1 synergistically boosts β-estradiol-induced proliferation and pro-angiogenesis of eutopic and ectopic endometrial stromal cells in adenomyosis.Reproductive biology and endocrinology : RB&E · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenomyosis (ADS) is a commonly encountered benign gynecological disorder. Epithelial-mesenchymal transition (EMT) may serve a pivotal role in the pathogenesis of ADS. Talin1 has been identified to be implicated in multiple human carcinomas, probably through inducing EMT process. However, available data on the precise molecular mechanism of Talin1 in the pathogenesis of ADS remain extremely scanty. In the present study, we aim to investigate the clinical roles of Talin1 and its effects on uterine endometrial cell migration, invasion, and EMT in ADS. Relative mRNA expression of Talin1, microRNA-145-5p (miR-145-5p), and EMT-related markers was determined by qRT-PCR. Immunohistochemistry and immunofluorescence were performed to examine the distribution of Talin1 in ADS endometrium. Protein levels of Talin1, EMT-related markers, and wnt/β-catenin pathway were measured by western blot. Wound healing assay and transwell assay were utilized for evaluating cell migration and invasion respectively. Dual-luciferase reporter assay was performed to verify the relationship between Talin1 and miR-145-5p. We found Talin1 was markedly overexpressed in ADS endometrial tissue and cells, whereas miR-145-5p was downregulated. Elevated Talin1 mRNA level might be closely related to some clinicopathological features of ADS. Through functional experiments, we demonstrated that overexpression of Talin1 induced EMT and enhanced migration and invasion ability of ADS eutopic and ectopic endometrial epithelial cells (ADS_Eu_EEC and ADS_Ec_EEC) in vitro through activating the canonical wnt/β-catenin pathway. From a mechanistic perspective, Talin1 was inversely regulated by miR-145-5p as a direct target. Our findings unveiled that under the regulation of miR-145-5p, Talin1 might promote endometrial cell migration and invasion through inducing EMT, presenting a novel insight for elucidating the pathogenesis of ADS.
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