ArticleCommunications biology2026
METTL3-mediated m6A modification of FDX1 confers resistance to cuproptosis and promotes hepatocellular carcinoma progression.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- Immunogenic cell death: synergizing ferroptosis and cuproptosis to overcome immunotherapy resistance.Medical oncology (Northwood, London, England) · 2026Review
- Harnessing copper-iron crosstalk: A novel strategy to combat hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- METTL14 Downregulation Accelerates HBV-Related Cirrhosis and Hepatocellular Carcinoma by Promoting Type I Interferon Release via the cGAS-STING Pathway Through mJournal of medical virology · 2026Article
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- Epigenetic regulation of cuproptosis in cancer: mechanisms, microenvironment, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Post-Translational Modification Networks in Ferroptosis: Orchestrating Defense, Drug Resistance, and Therapeutic Opportunities in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuproptosis, a copper-dependent cell death pathway, is emerging as a potential cancer treatment strategy. N6-methyladenosine (m6A), the predominant eukaryotic RNA modification, regulates various cell death mechanisms; however, its role in cuproptosis within hepatocellular carcinoma (HCC) remains unclear. Here, we found that METTL3 expression and m6A modification are upregulated during cuproptosis in HCC cells. Mechanistically, METTL3 mediated m6A modification of FDX1 mRNA, whereas the m6A reader FMR1 inhibited FDX1 translation. Consequently, METTL3 conferred resistance to cuproptosis by suppressing FDX1 protein expression in an m6A-FMR1-dependent manner. Knockdown or pharmacological inhibition of METTL3 sensitized HCC cells to elesclomol-Cu-induced cuproptosis and effectively suppressed HCC xenograft growth in vivo. Clinically, elevated METTL3 expression was associated with poor HCC prognosis, and the protein expression of METTL3 and FDX1 was negatively correlated in HCC tissues. In conclusion, our findings identify an METTL3-mediated m6A regulatory mechanism controlling cuproptosis sensitivity, revealing METTL3 inhibition as a promising therapeutic strategy 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.