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Hepatitis B Virus–Mediated m6A Demethylation Increases Hepatocellular Carcinoma Stemness and Immune Escape
Hepatitis B Virus Increases Liver Cancer Stem Cell Traits and Ability to Avoid the Immune System by Changing RNA Modifications
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Abstract
HBV infection is associated with downregulation of in HBV-positive hepatocellular carcinoma (HCC).
- The level of m6A modification is reduced in HBV-positive HCC due to increased stability of mRNA.
- ALKBH5 mRNA is necessary for maintaining stemness and self-renewal in HBV-positive HCC but not in HBV-negative HCC.
- ALKBH5 demethylates m6A modifications on the SNAI2 gene, leading to increased stability of SNAI2 transcripts.
- SNAI2 contributes to cancer stem cell traits in HBV-positive HCC and can reverse the effects of ALKBH5 knockdown.
- The ALKBH5/SNAI2 axis is linked to enhanced tumor immune evasion by activating the immune checkpoint ligand CD155.
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