ArticleBioMed research international2018
Autophagy Suppresses Invasiveness of Endometrial Cells through Reduction of Fascin-1.
Article in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 16 citations in OpenAlex.
- Fascin-Centred Invasive Competence in Eutopic Endometrium: A Hypothesis-Driven Narrative Review of Endometriosis Pathogenesis and Non-Surgical Biomarker Potential.International journal of molecular sciences · 2026Review
- Functional Analysis of the Histidine N-Methyltransferase SETD3 in Endometriosis.International journal of molecular sciences · 2026Article
- Dysregulated autophagy in endometriosis: molecular mechanisms, controversies, and clinical implications.Reproductive biology and endocrinology : RB&E · 2025Review
- Endometriosis and Cytoskeletal Remodeling: The Functional Role of Actin-Binding Proteins.Cells · 2025Review
- Prefoldin-5 Expression Is Elevated in Eutopic and Ectopic Endometriotic Epithelium and Modulates Endometriotic Epithelial Cell Proliferation and Migration In Vitro.International journal of molecular sciences · 2024Article
- CCL20/CCR6 axis mediates macrophages to promote proliferation and migration of ESCs by blocking autophagic flux in endometriosis.Stem cell research & therapy · 2022Article
- Role for autophagy-related markers Beclin-1 and LC3 in endometriosis.BMC women's health · 2022Article
- FSCN1 acts as a promising therapeutic target in the blockade of tumor cell motility: a review of its function, mechanism, and clinical significance.Journal of Cancer · 2022Review
- miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis.Molecular medicine reports · 2021Article
- Identification and Analysis of Potential Autophagy-Related Biomarkers in Endometriosis by WGCNA.Frontiers in molecular biosciences · 2021Article
- Vimentin intermediate filament assembly regulates fibroblast invasion in fibrogenic lung injury.JCI insight · 2019Article
- Role of Endometrial Autophagy in Physiological and Pathophysiological Processes.Journal of Cancer · 2019Review
- Inhibition of human glioblastoma cell invasion involves PION@E6 mediated autophagy process.Cancer management and research · 2019Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAutophagy has been reported to be involved in the development of various disorders such as neurodegenerative and metabolic diseases and tumors. Autophagy activators and inhibitors are also potential therapeutics for these diseases. However, the mechanism of autophagic involvement in different diseases is not the same, and the role of autophagy in endometriosis (EM) has not yet been elucidated. This research investigated the mechanism by which autophagy acts in EM, with the aim of establishing a theoretical basis for its prevention and treatment through the targeted interference with autophagy.
methodsWe used an RNA interference fragment targeting ATG5, the autophagy activator rapamycin, and the autophagy inhibitor 3-MA or overexpression of filopodia-related protein fascin-1, in conjunction with clonogenic assays, growth curves, and scratch assay to investigate the influence of autophagy on cellular growth, proliferation, and invasiveness. We collected specimens from 20 clinical cases of EM and investigated the protein expression of the autophagic marker LC3-II, the autophagic substrate p62, and fascin-1.
resultsRapamycin was able to inhibit the proliferation and colony formation of the endometriotic cell line CRL-7566, whereas the autophagy inhibitor 3-MA as well as the interference with the autophagy-related gene ATG5 had the opposite effect. More importantly, the autophagy activator rapamycin was able to inhibit the growth of filopodia in the endometriotic cells, and the overexpression of the fascin-1 restored the rapamycin-induced decrease of invasiveness. We found that the expression of the autophagy marker LC3-II was significantly reduced among the clinical EM specimens compared to the control group, while the expressions of fascin-1 and autophagic substrate p62 were increased.
conclusionOur results indicate that the inhibition of autophagy and exogenous expression of fascin-1 may promote the invasiveness of endometrial cells. As a corollary, autophagy represents a potential target for the treatment of EM.
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