ArticleCancers2022
FTO Inhibits Epithelial Ovarian Cancer Progression by Destabilising SNAI1 mRNA through IGF2BP2.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- IGF2BP3 promotes epithelial ovarian cancer progression by regulating FASN expression.Scientific reports · 2026Article
- m6A modification and its clinical applications in gynaecological cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- Fat mass and obesity-associated protein downregulation enhances N6-methyladenosine methylation and drives ovarian cancer progression.Journal of cell communication and signaling · 2025Article
- FTO degrader impairs ribosome biogenesis and protein translation in acute myeloid leukemia.Science advances · 2025Article
- Dual Disruption of EGFR/PI3K Signaling: IGF2BP2 Targeting Reverses Anti-EGFR Resistance in CAFs-Infiltrated Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).Molecular medicine reports · 2025Review
- Epigenetic regulation in female reproduction: the impact of m6A on maternal-fetal health.Cell death discovery · 2025Review
- Stabilization of SQLE mRNA by WTAP/FTO/IGF2BP3-dependent manner in HGSOC: implications for metabolism, stemness, and progression.Cell death & disease · 2024Article
- IGF2BP2 Shapes the Tumor Microenvironment by Regulating Monocyte and Macrophage Recruitment in Bladder Cancer.Cancer medicine · 2024Article
- Crosstalk Between m6A RNA Methylation and miRNA Biogenesis in Cancer: An Unholy Nexus.Molecular biotechnology · 2024Review
- Medicinal chemistry aspects of fat mass and obesity associated protein: structure, function and inhibitors.Future medicinal chemistry · 2024Review
- Synchronous profiling of mRNA N6-methyladenosine modifications and mRNA expression in high-grade serous ovarian cancer: a pilot study.Scientific reports · 2024Article
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- Regulation of ULK1 by WTAP/IGF2BP3 axis enhances mitophagy and progression in epithelial ovarian cancer.Cell death & disease · 2024Article
- Article
- Research progress on m6A demethylase FTO and its role in gynecological tumors.Frontiers in oncology · 2024Review
- Emerging role of m6A modification in ovarian cancer: progression, drug resistance, and therapeutic prospects.Frontiers in oncology · 2024Review
- RNA NCell communication and signaling : CCS · 2023Review
- Roles of RNA Methylations in Cancer Progression, Autophagy, and Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Fat mass and obesity-associated protein (FTO) regulates critical pathways in various diseases, including malignant tumours. However, the functional link between FTO and its target genes in epithelial ovarian cancer (EOC) development remains to be elucidated. In this study, the biological functions of FTO were verified in vitro and in vivo. The m6A modification and the binding sites of SNAI1 mRNA were confirmed by m6A RNA immunoprecipitation (MeRIP) and RIP experiments. The actinomycin D assay was used to test the stability of RNA. We found that FTO was downregulated with increased m6A levels in EOC. Reduced expression of FTO was associated with a higher FIGO stage in patients with EOC. Mechanistically, FTO decreased the m6A level and stability of SNAI1 mRNA, causing downregulation of SNAI1 and inhibiting epithelial-mesenchymal transition (EMT). Furthermore, FTO-mediated downregulation of SNAI1 expression depended on IGF2BP2, which acted as an m6A reader binding to the 3' UTR region of SNAI1 mRNA to promote its stability. In conclusion, FTO inhibits SNAI1 expression to attenuate the growth and metastasis of EOC cells in an m6A-IGF2BP2-dependent manner. Our findings suggest that the FTO-IGF2BP2-SNAI1 axis is a potential therapeutic target in EOC.
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What Socratic holds
Registered trials
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.