ArticleNature communications2015
Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 161 citations in OpenAlex.
- SETDB1 cooperates with the CRL4B complex to promote colorectal cancer tumorigenesis by disrupting circadian rhythm.Oncogene · 2026Article
- Article
- ITGB5 promotes immune escape in hepatocellular carcinoma by regulating PD-L1 through SETDB1/Hippo signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Targeting MORC2 activates transposable element-mediated viral mimicry and potentiates immune checkpoint blockade in triple-negative breast cancer.Molecular cancer · 2026Article
- Integrative Mapping of Regulatory Variation in African American Hepatocytes Using Colocalization and MPRA: Toward Precision Drug Response.Research square · 2026Article
- SETDB1 promotes gastric cancer progression via UPR and mTOR pathway.Cancer cell international · 2026Article
- The Many Faces of SetDB1.Epigenomes · 2026Review
- Dual Aptamers-Based SETDB1 PROTACs as Effective Anti-Tumor Strategies for Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Functional Analyses of Histone Methyltransferases in Sea Lamprey Embryos Undergoing Programmed DNA Elimination.bioRxiv : the preprint server for biology · 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
- SETDB1 is critically required for uveal melanoma growth and represents a promising therapeutic target.Cell death & disease · 2025Article
- Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.The Kaohsiung journal of medical sciences · 2025Review
- Identification and clinical implications of endogenous retrovirus elements suppressed by SETDB1 in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- Potent and selective SETDB1 covalent negative allosteric modulator reduces methyltransferase activity in cells.Nature communications · 2025Article
- Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy.Current cancer drug targets · 2025Review
- SETDB1: an emerging target for anticancer drug development.Future medicinal chemistry · 2025Article
- MicroRNA-409: Molecular functions and clinical applications in cancer.Biochemistry and biophysics reports · 2024Review
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- Cytoplasmic localization of SETDB1‑induced Warburg effect via c‑MYC‑LDHA axis enhances migration and invasion in breast carcinoma.International journal of molecular medicine · 2024Article
- LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling.Molecular cancer · 2024Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SETDB1 is a histone H3K9 methyltransferase that has a critical role in early development. It is located within a melanoma susceptibility locus and facilitates melanoma formation. However, the mechanism by which SETDB1 regulates tumorigenesis remains unknown. Here we report the molecular interplay between SETDB1 and the well-known hotspot gain-of-function (GOF) TP53 R249S mutation. We show that in hepatocellular carcinoma (HCC) SETDB1 is overexpressed with moderate copy number gain, and GOF TP53 mutations including R249S associate with this overexpression. Inactivation of SETDB1 in HCC cell lines bearing the R249S mutation suppresses cell growth. The TP53 mutation status renders cancer cells dependent on SETDB1. Moreover, SETDB1 forms a complex with p53 and catalyses p53K370 di-methylation. SETDB1 attenuation reduces the p53K370me2 level, which subsequently leads to increased recognition and degradation of p53 by MDM2. Together, we provide both genetic and biochemical evidence for a mechanism by which SETDB1 regulates cancer cell growth via methylation of p53.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.