ArticleThe Journal of biological chemistry2013
DNA double-strand breaks lead to activation of hypermethylated in cancer 1 (HIC1) by SUMOylation to regulate DNA repair.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 44 citations in OpenAlex.
- SUMOylation Protects Endothelial Cell-Expressed Leukocyte-Specific Protein 1 from Ubiquitination-Mediated Proteasomal Degradation and Facilitates Its Nuclear Export.International journal of molecular sciences · 2026Article
- Crosstalk between SUMOylation and other post-translational modifications in breast cancer.Cellular & molecular biology letters · 2024Review
- Aging Hallmarks and Progression and Age-Related Diseases: A Landscape View of Research Advancement.ACS chemical neuroscience · 2024Review
- SUMOylation of zebrafish transcription factor Zbtb21 affects its transcription activity.PeerJ · 2024Article
- Effect of Diet and Oxidative Stress in the Pathogenesis of Lymphoproliferative Disorders.Antioxidants (Basel, Switzerland) · 2023Review
- Multifaceted Influence of Histone Deacetylases on DNA Damage Repair: Implications for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2023Review
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Aging-associated accumulation of mitochondrial DNA mutations in tumor origin.Life medicine · 2022Review
- Targeting Redox Regulation as a Therapeutic Opportunity against Acute Leukemia: Pro-Oxidant Strategy or Antioxidant Approach?Antioxidants (Basel, Switzerland) · 2022Review
- Metastasis-associated protein 1: A potential driver and regulator of the hallmarks of cancer.Journal of biosciences · 2022Review
- New insights of epigenetics in vascular and cellular senescence.Journal of translational internal medicine · 2021Review
- HIC1 Represses Atoh1 Transcription and Hair Cell Differentiation in the Cochlea.Stem cell reports · 2021Article
- The significant role of redox system in myeloid leukemia: from pathogenesis to therapeutic applications.Biomarker research · 2020Review
- Article
- hPCL3S promotes proliferation and migration of androgen-independent prostate cancer cells.Oncotarget · 2020Article
- Metformin and tenovin-6 synergistically induces apoptosis through LKB1-independent SIRT1 down-regulation in non-small cell lung cancer cells.Journal of cellular and molecular medicine · 2019Article
- A new method for constructing tumor specific gene co-expression networks based on samples with tumor purity heterogeneity.Bioinformatics (Oxford, England) · 2018Article
- Article
- SUMO, a small, but powerful, regulator of double-strand break repair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIC1 (hypermethylated in cancer 1) is a tumor suppressor gene frequently epigenetically silenced in human cancers. HIC1 encodes a transcriptional repressor involved in the regulation of growth control and DNA damage response. We previously demonstrated that HIC1 can be either acetylated or SUMOylated on lysine 314. This deacetylation/SUMOylation switch is governed by an unusual complex made up of SIRT1 and HDAC4 which deacetylates and thereby favors SUMOylation of HIC1 by a mechanism not yet fully deciphered. This switch regulates the interaction of HIC1 with MTA1, a component of the NuRD complex and potentiates the repressor activity of HIC1. Here, we show that HIC1 silencing in human fibroblasts impacts the repair of DNA double-strand breaks whereas ectopic expression of wild-type HIC1, but not of nonsumoylatable mutants, leads to a reduced number of γH2AX foci induced by etoposide treatment. In this way, we demonstrate that DNA damage leads to (i) an enhanced HDAC4/Ubc9 interaction, (ii) the activation of SIRT1 by SUMOylation (Lys-734), and (iii) the SUMO-dependent recruitment of HDAC4 by SIRT1 which permits the deacetylation/SUMOylation switch of HIC1. Finally, we show that this increase of HIC1 SUMOylation favors the HIC1/MTA1 interaction, thus demonstrating that HIC1 regulates DNA repair in a SUMO-dependent way. Therefore, epigenetic HIC1 inactivation, which is an early step in tumorigenesis, could contribute to the accumulation of DNA mutations through impaired DNA repair and thus favor tumorigenesis.
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