ArticleJournal of translational medicine2023
METTL3-mediated m6A modification of SIRT1 mRNA inhibits progression of endometriosis by cellular senescence enhancing.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Icaritin improves pregnancy outcomes in endometriosis by inhibiting ovarian granulosa cell senescence.Molecular biology reports · 2026Article
- METTL3 Regulates the Senescence of Stem Cells From the Apical Papilla by Mediating the mInternational dental journal · 2026Article
- Advances in m6A Modification in Pregnancy-Related Disorders and Female Reproductive Endocrine Diseases.Expert reviews in molecular medicine · 2026Review
- The Role of NMedComm · 2026Review
- SIRT1-mediated deacetylation of HMGB1 promotes the progression of endometriosis by regulating autophagy.Scientific reports · 2026Article
- Unravelling Multilayered RNA Modification Networks in Female Reproduction and Obstetric/Gynaecologic Disorders.Biomolecules · 2026Review
- Senescence-Driven Remodeling Defines an Aggressive and Immunomodulatory Subtype of Endometriosis.Aging cell · 2026Article
- SETD7 regulates decidual senescence through FOXO1-dependent mechanisms in human endometrial stromal cells.Journal of assisted reproduction and genetics · 2026Article
- The role of mGenes & diseases · 2026Review
- m6A Methyltransferase METTL3 Regulates Inflammatory and Immune Microenvironments in Renal Cell Carcinoma via Modulation of the PI3K/AKT Pathway.International journal of genomics · 2026Article
- Molecular Regulation of FOXO1 and Its Pathophysiological Significance in Endometriosis: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Sirtuins in Women's Health.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Nexus of Iron, Senescence, and Fibrosis in Endometriosis: A Narrative Review.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- The Role of the Microbiome in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Phospholipase Cε1 activates Rap1 signaling pathway to promote proliferation, EMT and angiogenesis of choriocarcinoma cells.Molecular biology reports · 2025Article
- Review
- Understanding epigenetic regulation in the endometrium - lessons from mouse models with implantation defects.Epigenomics · 2025Review
- Multiomic insight into the involvement of cell aging related genes in the pathogenesis of endometriosis.Scientific reports · 2025Article
- A novel mechanism of FTO modulating the progression of endometriosis through mediating the m6A methylation of GEF-H1 in a YTHDF1-dependent manner.Molecular medicine (Cambridge, Mass.) · 2025Article
- METTL3 blocked the progression of diabetic retinopathy through m6A-modified SOX2.Open medicine (Warsaw, Poland) · 2025Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndometriosis (EMs), the ectopic planting of functional endometrium outside of the uterus, is a leading cause of infertility and pelvic pain. As a fundamental mRNA modification, N6-methyladenosine (m6A) participates in various pathological processes. However, the role of m6A RNA modification in endometriosis remains unclear. The present study explores METTL3-mediated m6A modification and the mechanisms involved in endometriosis.
methodsThe dominant m6A regulators in EMs were analysed using RT‒PCR. Candidate targets and possible mechanisms of METTL3 were assessed by m6A-mRNA epitranscriptomic microarray and RNA sequencing. A primary ESCs model was employed to verify the effect of METTL3 on m6A modification of SIRT1 mRNA, and the mechanism was elucidated by RT‒PCR, Western blotting, MeRIP, and RIP assays. CCK-8 viability assays, Transwell invasion assays, EdU proliferation assays, wound healing migration assays, and senescence-associated β-galactosidase staining were performed to illuminate the potential biological mechanism of METTL3 and SIRT1 in ESCs in vitro. An in vivo PgrCre/ + METTL3 -/- female homozygous mouse model and a nude mouse xenograft model were employed to further investigate the physiologic consequences of METTL3-mediated m6A alteration on EMs.
resultsOur data show that decreased METTL3 expression significantly downregulates m6A RNA methylation levels in ESCs. Silencing m6A modifications mediated by METTL3 accelerates ESCs viability, proliferation, migration, and invasion in vitro. The m6A reader protein YTHDF2 binds to m6A modifications to induce the degradation of SIRT1 mRNA. SIRT1/FOXO3a signalling pathway activation is subsequently inhibited, promoting the cellular senescence of ESCs and inhibiting the ectopic implantation of ESCs in vitro and in vivo.
conclusionsOur findings demonstrate that METTL3-mediated m6A methylation epigenetically regulates the ectopic implantation of ESCs, resulting in the progression of endometriosis. Our study establishes METTL3-YTHDF2-SIRT1/FOXO3a as a critical axis and potential mechanism in endometriosis.
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