ArticleScientific reports2019
CHD4 regulates the DNA damage response and RAD51 expression in glioblastoma.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Role of CHD4 in tumor progression, DNA damage response and treatment resistance (Review).Oncology reports · 2026Review
- High-throughput radiation sensitivity screening of 3D-head and neck squamous cell carcinoma (HNSCC) organoids using an automated radiation modulator (ARM).Materials today. Bio · 2026Article
- CHD4 epigenetically coordinates genomic instability and immunosuppression to drive pan-cancer progression and confer HDAC inhibitor sensitivity.Clinical and experimental medicine · 2026Article
- The NuRD chromatin remodeling complex contributes to repairing exogenous double-strand breaks in the Caenorhabditis elegans germline.Genetics · 2026Article
- CHD4 and NOX4 expression in thyroid tumor tissues.Exploration of targeted anti-tumor therapy · 2026Article
- NuRD chromatin remodeling is required to repair exogenous DSBs in thebioRxiv : the preprint server for biology · 2025Article
- Proteomic Analysis Uncovers Enhanced Inflammatory Phenotype and Distinct Metabolic Changes in IDH1 Mutant Glioma Cells.International journal of molecular sciences · 2025Article
- Synergistic enhancement of PARP inhibition via small molecule UNI66-mediated suppression of BRD4-dependent transcription ofNAR cancer · 2025Article
- Repurposing Linezolid in Conjunction with Histone Deacetylase Inhibitor Access in the Realm of Glioblastoma Therapies.Journal of medicinal chemistry · 2025Article
- The Roles of H3K9me3 Writers, Readers, and Erasers in Cancer Immunotherapy.International journal of molecular sciences · 2024Review
- CRISPR-Cas9 knockout screen identifies novel treatment targets in childhood high-grade glioma.Clinical epigenetics · 2023Article
- Hyperglycemia-Suppressed SMARCA5 Disrupts Transcriptional Homeostasis to Facilitate Endothelial Dysfunction in Diabetes.Diabetes & metabolism journal · 2023Article
- CHD4 is recruited by GATA4 and NKX2-5 to repress noncardiac gene programs in the developing heart.Genes & development · 2022Article
- Identification of Tissue Types and Gene Mutations From Histopathology Images for Advancing Colorectal Cancer Biology.IEEE open journal of engineering in medicine and biology · 2022Article
- ZERO-INFLATED QUANTILE RANK-SCORE BASED TEST (ZIQRANK) WITH APPLICATION TO SCRNA-SEQ DIFFERENTIAL GENE EXPRESSION ANALYSIS.The annals of applied statistics · 2021Article
- Sentinels of chromatin: chromodomain helicase DNA-binding proteins in development and disease.Genes & development · 2021Review
- Expression Levels of RAD51 Inversely Correlate with Survival of Glioblastoma Patients.Cancers · 2021Article
- Histone deacetylase 6 acts upstream of DNA damage response activation to support the survival of glioblastoma cells.Cell death & disease · 2021Article
- Article
- Regulation of RAD51 at the Transcriptional and Functional Levels: What Prospects for Cancer Therapy?Cancers · 2021Review
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9 authors.
Funding
Abstract
Glioblastoma (GBM) is a lethal brain tumour. Despite therapy with surgery, radiation, and alkylating chemotherapy, most people have recurrence within 6 months and die within 2 years. A major reason for recurrence is resistance to DNA damage. Here, we demonstrate that CHD4, an ATPase and member of the nucleosome remodelling and deactetylase (NuRD) complex, drives a component of this resistance. CHD4 is overexpressed in GBM specimens and cell lines. Based on The Cancer Genome Atlas and Rembrandt datasets, CHD4 expression is associated with poor prognosis in patients. While it has been known in other cancers that CHD4 goes to sites of DNA damage, we found CHD4 also regulates expression of RAD51, an essential component of the homologous recombination machinery, which repairs DNA damage. Correspondingly, CHD4 suppression results in defective DNA damage response in GBM cells. These findings demonstrate a mechanism by which CHD4 promotes GBM cell survival after DNA damaging treatments. Additionally, we found that CHD4 suppression, even in the absence of extrinsic treatment, cumulatively increases DNA damage. Lastly, we found that CHD4 is dispensable for normal human astrocyte survival. Since standard GBM treatments like radiation and temozolomide chemotherapy create DNA damage, these findings suggest an important resistance mechanism that has therapeutic implications.
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