ArticleCell reports. Medicine2026
Histone methyl-transferase G9a inhibition boosts the efficacy of immune checkpoint inhibitors in experimental hepatocellular carcinoma.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Inducing tumor-intrinsic innate immune response to break cancer immunotherapy resistance.Frontiers in medicine · 2026Review
- Molecular reprogramming in cutaneous melanoma: the central role of G9a and EZH2 methyltransferase inhibitors in tumor plasticity, immune evasion, and therapeutic resistance.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors.
Funding
Abstract
Immune checkpoint inhibitors (ICIs) transform cancer therapy, but their efficacy in hepatocellular carcinoma (HCC) remains limited due to tumor-intrinsic immune evasion. We investigate the epigenetic regulator G9a (EHMT2) as a driver of immune resistance and evaluate pharmacologic inhibition as a therapeutic strategy. G9a expression is analyzed across human HCC cohorts and correlated with transcriptomic signatures predictive of ICI response. Using human and murine HCC cell lines and immunocompetent mouse models, we assess the antitumor effects of two G9a inhibitors, CM272 and EZM8266, combined with anti-PD1 therapy. Elevated G9a expression inversely correlates with immune-related signatures of ICI responsiveness. G9a inhibition restores interferon gamma (IFN-γ) signaling, increases major histocompatibility complex (MHC) class I expression, enhances CXCL10-mediated T cell recruitment, and induces viral mimicry via derepression of endogenous retroviral elements and cytosolic double-stranded RNA (dsRNA) accumulation. In vivo, G9a inhibition synergizes with anti-PD1 therapy, suppresses tumor growth, and enhances CD8
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