ReviewFrontiers in cell and developmental biology2024
The function of histone methyltransferase SETDB1 and its roles in liver cancer.
Review in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SETDB1 cooperates with the CRL4B complex to promote colorectal cancer tumorigenesis by disrupting circadian rhythm.Oncogene · 2026Article
- ITGB5 promotes immune escape in hepatocellular carcinoma by regulating PD-L1 through SETDB1/Hippo signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Unveiling membrane transporter proteins-related genes for predicting the prognosis of hepatocellular carcinoma patients.Discover oncology · 2026Article
- The epigenetic regulator SETDB1 as a key component of cancer stem cells and drug resistance in primary liver cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Expression landscape of epigenetic genes in human hepatocellular carcinoma.Journal of physiology and biochemistry · 2025Article
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Authors and funding
2 authors.
Funding
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Abstract
Epigenetic alterations in gene expression have been implicated in cancer development and tumor immune escape, with posttranslational histone or non-histone modifications representing attractive targets for disease surveillance and therapy. SET domain bifurcated 1 (SETDB1) is a histone lysine methyltransferase that reversibly catalyzes the di- and tri-methylation of histone 3 lysine 9 (H3K9) on euchromatin, inhibiting gene transcription within these regions and facilitating the switch from euchromatic to heterochromatic states. Emerging evidence suggests that SETDB1 amplification and aberrant activation are significantly associated with poor prognosis in hepatocellular carcinoma (HCC), and contribute to HCC development, immune escape, and immune checkpoint blockade (ICB) resistance. Here, we provide an updated overview of the cellular and molecular effects of SETDB1 activity in hepatocarcinogenesis and progression and focus on studies linking its function to immunotherapy for HCC, and present current challenges and future perspectives for targeting SETDB1 in HCC treatment.
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