ArticleScientific reports2025
The m6A reader IGF2BP3 promotes HCC progression by enhancing MCM10 stability.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed.
- IGF2BP3 enhances paclitaxel resistance in bladder urothelial carcinoma by recognizing mMedical oncology (Northwood, London, England) · 2026Article
- IGF2BP3 in Multi-System Diseases: Molecular Mechanisms, Pathological Roles and Translational Insights.Cell biochemistry and biophysics · 2026Review
- Identification of MARCKSL1 as an independent prognostic biomarker and analysis of its potential regulatory network in hepatocellular carcinoma.Discover oncology · 2026Article
- Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Recent advances in m6A RNA modification in hepatocellular carcinoma: from mechanisms to therapeutic potential.Frontiers in molecular biosciences · 2026Review
- IGF2BP3 redirects glycolytic flux to promote one-carbon metabolism and RNA methylation.Cell reports · 2025Article
- mMolecules (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Abnormal N6-methyladenosine (m6A) modifications were associated with the occurrence, development, and metastasis of cancer. However, the functions and mechanisms of m6A regulators in cancer remained largely elusive and should be explored. Here, we identified that insulin like growth Factor 2 mRNA binding protein 3 (IGF2BP3) was specifically overexpressed and associated with poor prognosis in liver hepatocellular carcinoma (HCC). Importantly, IGF2BP3 promoted HCC cells progression in an m6A-dependent manner, IGF2BP3 silencing significantly inhibited proliferation and migratory ability of tumor cells in vitro and in in vivo. Mechanistically, IGF2BP3 interacted with minichromosomal maintenance complex component (MCM10) mRNAs to prolong stability of m6A-modified RNA. Therefore, our findings indicated that m6A reader IGF2BP3 contributed to tumorigenesis and poor prognosis, providing a potential prognostic biomarker and therapeutic target for HCC.
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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.