ArticleAmerican journal of cancer research2026
PRMT5 inhibits the ferroptosis of hepatocellular carcinoma via regulating RBM15/FTH1 signaling.
Article in American journal of cancer research, 2026. 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.
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Who cites it
1 citing paper in PubMed.
- Histone Post-Translational Modifications Regulating Ferroptosis: The Molecular Mechanisms and Disease Associations.Cell biochemistry and function · 2026Review
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Authors and funding
7 authors.
Funding
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Abstract
Hepatocellular carcinoma (HCC) is one of the most malignant tumors worldwide. This study aimed to investigate the role of protein arginine methyltransferase 5 (PRMT5) in HCC. Gene expression was determined using reverse transcription-quantitative polymerase chain reaction, Western blot, and immunohistochemistry. The interaction between genes were determined using chromatin immunoprecipitation, glutathione-S-transferase pull-down, co-immunoprecipitation, and luciferase assays. m6A levels were determined using m6A dot assay. N6-methyladenosine (m6A) enrichment was determined using methylated RNA immunoprecipitation assay. Cellular functions were determined using Cell Counting Kit-8 assay and propidium iodide staining. Xenograft assay was conducted to further verify the role of PRMT5 in HCC. We found that overexpressed PRMT5 was upregulated in tumor protein p53 (TP53)-mutated HCC patients. TP53 epigenetically in activated PRMT5. PRMT5 deficiency promoted the ferroptosis of HCC cells
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