ArticleOncology research2025
N6-Methyladenosine Promotes the Transcription of c-Src Kinase via IRF1 to Facilitate the Proliferation of Liver Cancer.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
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Who cites it
1 citing paper in PubMed.
- Recent advances in m6A RNA modification in hepatocellular carcinoma: from mechanisms to therapeutic potential.Frontiers in molecular biosciences · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Expression of mRNA is widely regulated by N6-methyladenosine (m Methods: The correlation expression between c-Src and METTL3 between liver cancer patients and the control group was analyzed using the TCGA database, and was further demonstrated by Western blot and RT-qPCR. The functional roles of c-Src in METTL3-regulated liver cancer progression were investigated by cell proliferation assays and colony formation assays. The regulatory mechanism of METTL3 in c-Src expression was accessed by RNA-immunoprecipitation (RIP)-qPCR. Results: We demonstrated that c-Src kinase promoted liver cancer development, and the expression of Conclusion: Results suggested that the METTL3/IRF1/c-Src axis played potential oncogenic roles in liver cancer development and the axis may be a promising therapeutic target in the disease.
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