ArticleCell death discovery2021
METTL3 promotes the initiation and metastasis of ovarian cancer by inhibiting CCNG2 expression via promoting the maturation of pri-microRNA-1246.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- Emerging roles of mJournal of assisted reproduction and genetics · 2026Review
- Pseudouridine synthase 7 as a context-specific therapeutic target in cancer.The Journal of pharmacology and experimental therapeutics · 2026Review
- Epitranscriptomic Regulation of Platinum Resistance via the METTL3-ADAM23 Axis in Ovarian Cancer.Cells · 2026Article
- Molecular Insights into Widespread Pseudouridine RNA Modifications: Implications for Women's Health and Disease.Biology · 2026Review
- MicroRNA chemical modifications in post-transcriptional gene silencing and human diseases.Molecular therapy. Nucleic acids · 2025Review
- METTL3-mediated m6A modification of LINC00857 enhances stemness and metastasis of ovarian cancer cells by activating the YAP-TEAD pathway.Scientific reports · 2025Article
- Epigenetics in Ovarian Cancer: A Review of Current Knowledge and Future Perspectives.Biomedicines · 2025Review
- Sulforaphane: a natural organosulfur having potential to modulate apoptosis and survival signalling in cancer.Discover oncology · 2025Review
- IGF2BP2 binding to CPSF6 facilitates m6A-mediated alternative polyadenylation of PUM2 and promotes malignant progression in ovarian cancer.Clinical and translational medicine · 2025Article
- MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells.Scientific reports · 2025Article
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
- Inhibition of Mettl3 alleviates low-dose cisplatin-induced renal fibrosis and enhances the chemotherapeutic efficacy in mouse models of cancer.International journal of biological sciences · 2025Article
- Gut microbiota-derived metabolite phenylacetylglutamine inhibits the progression of prostate cancer by suppressing the Wnt/β-catenin signaling pathway.Frontiers in pharmacology · 2025Article
- Extracellular vesicles from highly invasive melanoma subpopulations increase the invasive capacity of less invasive melanoma cells through mir-1246-mediated inhibition of CCNG2.Cell communication and signaling : CCS · 2024Article
- METTL3 as a master regulator of translation in cancer: mechanisms and implications.NAR cancer · 2024Review
- mJournal of translational medicine · 2024Article
- The role of the methyltransferase METTL3 in prostate cancer: a potential therapeutic target.BMC cancer · 2024Review
- Emerging role of m6A modification in ovarian cancer: progression, drug resistance, and therapeutic prospects.Frontiers in oncology · 2024Review
- RNA modifications in gynecological cancer: current status and future directions.Frontiers in medicine · 2024Review
- LncRNA MALAT1 signaling pathway and clinical applications in overcome on cancers metastasis.Clinical and experimental medicine · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer is a common gynecological malignant tumor with a high mortality rate and poor prognosis. There is inadequate knowledge of the molecular mechanisms underlying ovarian cancer. We examined the expression of methyltransferase-like 3 (METTL3) in tumor specimens using RT-qPCR, immunohistochemistry, and Western blot analysis, and tested the methylation of METTL3 by MSP. Levels of METTL3, miR-1246, pri-miR-1246 and CCNG2 were then analyzed and their effects on cell biological processes were also investigated, using in vivo assay to validate the in vitro findings. METTL3 showed hypomethylation and high expression in ovarian cancer tissues and cells. Hypomethylation of METTL3 was pronounced in ovarian cancer samples, which was negatively associated with patient survival. Decreased METTL3 inhibited the proliferation and migration of ovarian cancer cells and promoted apoptosis, while METTL3 overexpression exerted opposite effects. Mechanistically, METTL3 aggravated ovarian cancer by targeting miR-1246, while miR-1246 targeted and inhibited CCNG2 expression. High expression of METTL3 downregulated CCNG2, promoted the metabolism and growth of transplanted tumors in nude mice, and inhibited apoptosis. The current study highlights the promoting role of METTL3 in the development of ovarian cancer, and presents new targets for its treatment.
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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 OpenQuestion graph.