ArticleScientific reports2025
IL35 modulates HBV-related HCC progression via IL6-STAT3 signaling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Processing enhances the anti-hepatocellular carcinoma effect of Momordicae Semen via remodeling chemical composition and regulating the Akt/mTOR/STAT3 pathway.Biochemistry and biophysics reports · 2026Article
- Induction of senescence like macrophages by hepatocellular carcinoma cells in vitro.Discover oncology · 2026Article
- Review
- Long-read sequencing reveals HBV integration patterns and oncogenic impact on early-onset hepatocellular carcinoma.Genome research · 2025Article
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Authors and funding
3 authors.
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Abstract
Hepatocellular carcinoma (HCC) is a common malignant tumor with incidences reported worldwide along with high mortality rates. It is a significant public health concern as hepatitis B virus (HBV) infection is the leading cause of HCC. IL35, a novel heterodimeric cytokine belonging to the IL-12 family, comprises two subunits, namely IL-12p35 and Epstein-Barr virus-induced gene 3 (EBI3). They are crucial in regulating immune responses to tumors and infectious diseases. However, their function in HBV-related HCC is unclear. The objective of this study was to identify the regulatory role of IL35 in the occurrence of HBV-related HCC and its underlying molecular mechanisms. The expression of IL35 was enhanced in human HBV-related HCC tissues. HBV induction, particularly HBx, enhanced the expression of IL-35 in hepatoma cell lines. Silencing IL-35 promoted apoptosis and suppressed proliferation, cell cycle progression, migration, and invasion of HBx-induced hepatoma cells. Mechanistically, silencing IL-35 effectively inhibited the activation of the IL-6-STAT3 signaling pathway by suppressing the expression of IL-6 and nuclear import and phosphorylation of STAT3 in HBx-induced hepatoma cells. Therefore, inhibiting the IL6-STAT3 signaling pathway by silencing IL35 effectively alleviated the progression of HBV-related HCC. IL35 is a potential target for treating HBV-related HCC.
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