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Topics {✒️}

month download article/chapter hepatocyte ikkß/nf prostaglandin a2-mediated stabilization anti-viral protein apobec3g erk-dependent pathway requiring jak1/stat3 signaling pathway rna-binding protein hur multiple human cancers dna-reactive carcinogens 2-acetylaminofluorene central college fund liver cancer progenitors t-cell intracellular antigen-1 tumor-derived hepatocyte rat liver carcinogenesis full article pdf hepatocellular carcinoma cells china life sci diverse apobec proteins apobec3 editing enzymes massive apobec3 editing privacy choices/manage cookies inhibits tumor promotion mammary epithelial cells serous ovarian carcinoma jiangsu key laboratory hur regulates cyclin apobec3 proteins expressed apobec3 family proteins virus transgenic mice interferon-inducible expression cancer-related inflammation related subjects china pharmaceutical university hepatocellular carcinoma potential prognostic biomarker global cancer statistics european economic area activating mtor signaling tnfa 3’-untranslated region milk-borne virions impair genomic stability inducing base substitutions il-6 mrna stability potential therapeutic target conditions privacy policy dna cytidine deaminase cytidine deamination inflammatory cytokines promote drug safety evaluation hematopoietic cell subsets

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• Hepatocyte IKKß/NF-?

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         headline:APOBEC3B and IL-6 form a positive feedback loop in hepatocellular carcinoma cells
         description:APOBEC3 protein families, a DNA cytidine deaminase, were up-regulated in multiple tumors. However, the relationship between Hepatocellular carcinoma (HCC) and APOBEC3B (A3B) remains unknown. It has been confirmed that interleukin-6 (IL-6) has significant impacts on oncogenesis of HCC. Here, we reported that the expression of IL-6 was substantially up-regulated by A3B in HepG2 cells. A3B induced IL-6 expression through relocating HuR to enhance the IL-6 mRNA stability. Further analysis indicated that IL-6 also increased the expression of A3B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3B and IL-6, and thereby promoted the prolonged non-resolving inflammation. Collectively, these findings suggest that A3B is essential for oncogenesis of HCC, and is a potential target for preventive intervention.
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      headline:APOBEC3B and IL-6 form a positive feedback loop in hepatocellular carcinoma cells
      description:APOBEC3 protein families, a DNA cytidine deaminase, were up-regulated in multiple tumors. However, the relationship between Hepatocellular carcinoma (HCC) and APOBEC3B (A3B) remains unknown. It has been confirmed that interleukin-6 (IL-6) has significant impacts on oncogenesis of HCC. Here, we reported that the expression of IL-6 was substantially up-regulated by A3B in HepG2 cells. A3B induced IL-6 expression through relocating HuR to enhance the IL-6 mRNA stability. Further analysis indicated that IL-6 also increased the expression of A3B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3B and IL-6, and thereby promoted the prolonged non-resolving inflammation. Collectively, these findings suggest that A3B is essential for oncogenesis of HCC, and is a potential target for preventive intervention.
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