ArticleReproductive sciences (Thousand Oaks, Calif.)2022
N6-methyladenosine Demethylase FTO Induces the Dysfunctions of Ovarian Granulosa Cells by Upregulating Flotillin 2.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 36 citations in OpenAlex.
- Emerging roles of mJournal of assisted reproduction and genetics · 2026Review
- Advances in m6A Modification in Pregnancy-Related Disorders and Female Reproductive Endocrine Diseases.Expert reviews in molecular medicine · 2026Review
- FTO-mediated NR1D1 mScientific reports · 2026Article
- Unravelling Multilayered RNA Modification Networks in Female Reproduction and Obstetric/Gynaecologic Disorders.Biomolecules · 2026Review
- Integrative bioinformatics, single-cell and experimental evidence for a BPA-m6A-apoptosis axis in granulosa cell dysfunction in polycystic ovary syndrome.Journal of ovarian research · 2026Article
- The Intersection of m6A Methylation and Immune Response in PCOS: A Bioinformatics Perspective.Immunity, inflammation and disease · 2026Article
- The role of mGenes & diseases · 2026Review
- Epitranscriptomic regulation via m6A RNA modification in PCOS pathophysiology.Molecular biology reports · 2025Review
- Research progress on m6A RNA methylation modification in human reproduction related diseases.European journal of medical research · 2025Review
- Mechanism of crosstalk between DNA methylation and histone acetylation and related advances in diagnosis and treatment of premature ovarian failure.Epigenetics · 2025Review
- YTHDC1 Promoted Cell Proliferation and Decidualization by Maintaining Nuclear C/EBPβ Stability in Decidual Stromal Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Comprehensive analysis of cuproptosis and m6A-Target gene signatures for diagnostic significance and immune microenvironment characterization in polycystic ovary syndrome.Scientific reports · 2025Article
- The emerging roles of N6-methyladenosine (m6A) deregulation in polycystic ovary syndrome.Journal of ovarian research · 2025Review
- Epigenetic regulation in female reproduction: the impact of m6A on maternal-fetal health.Cell death discovery · 2025Review
- Role of epigenetic regulation in diminished ovarian reserve.Journal of assisted reproduction and genetics · 2025Review
- Research progress on the pathogenesis, clinical impact, and traditional Chinese medicine treatment of polycystic ovary syndrome complicated by insulin resistance.Frontiers in pharmacology · 2025Review
- Epigenetic regulation in oogenesis and fetal development: insights into m6A modifications.Frontiers in immunology · 2025Review
- HNRNPH1 stabilizes FLOT2 mRNA in a non-canonical m6A-dependent manner to promote malignant progression in nasopharyngeal carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- NImmunity, inflammation and disease · 2024Review
- The Role of N6-methyladenosine Modification in Gametogenesis and Embryogenesis: Impact on Fertility.Genomics, proteomics & bioinformatics · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovarian syndrome (PCOS) is often accompanied by overweight/obesity and insulin resistance. The dysfunctions of ovarian granulosa cells (GCs) are closely linked with the pathogenesis of PCOS. Fat mass and obesity-associated gene (FTO), an N6-methyladenosine (m6A) demethylase, has been reported to be implicated in the risks and insulin resistance of PCOS. However, the roles of FTO in the development of GCs along with its m6A-related regulatory mechanisms are poorly defined. Cell proliferative ability was detected by MTT assay. Cell apoptotic rate was measured via flow cytometry. Insulin resistance was assessed by GLUT4 transport potential. The mRNA and protein levels of FTO and flotillin 2 (FLOT2) were determined by RT-qPCR and western blot assays, respectively. FLOT2 was screened out to be a potential FTO target through differential expression analysis for the GSE95728 dataset and target prediction analysis by POSTAR2 and STARBASE databases. The interaction between FTO and FLOT2 was analyzed by RNA immunoprecipitation (RIP) assay. The effect of FTO upregulation on FLOT2 m6A level was measured by methylated RIP (meRIP) assay. FLOT2 mRNA stability was examined by actinomycin D assay. FTO overexpression facilitated cell proliferation, hindered cell apoptosis, and induced insulin resistance in GCs. FTO promoted FLOT2 expression by reducing m6A level on FLOT2 mRNA and increasing FLOT2 mRNA stability. FLOT2 loss weakened the effects of FTO overexpression on cell proliferation/apoptosis and insulin resistance in GCs. FTO induced the dysfunctions of GCs by upregulating FLOT2, suggesting that FTO/FLOT2 might play a role in the pathophysiology of PCOS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.