ArticleScientific reports2019
CHD7 promotes glioblastoma cell motility and invasiveness through transcriptional modulation of an invasion signature.
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 16 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
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- Comprehensive Analysis of the Expression, Prognosis, and Immune Infiltrates for Chromodomain-Helicase-DNA-Binding Proteins in Breast Tumor.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- The therapeutic potential of targeting the CHD protein family in cancer.Pharmacology & therapeutics · 2024Review
- Evaluation of drug sensitivity, immunological characteristics, and prognosis in melanoma patients using an endoplasmic reticulum stress-associated signature based on bioinformatics and pan-cancer analysis.Journal of molecular medicine (Berlin, Germany) · 2023Article
- The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer.Cancer research · 2023Article
- Immunological and tumor-intrinsic mechanisms mediate the synergistic growth suppression of experimental glioblastoma by radiotherapy and MET inhibition.Acta neuropathologica communications · 2023Article
- Targeted Epigenetic Interventions in Cancer with an Emphasis on Pediatric Malignancies.Biomolecules · 2022Review
- Activation of Oncogenic and Immune-Response Pathways Is Linked to Disease-Specific Survival in Merkel Cell Carcinoma.Cancers · 2022Article
- Comprehensive analysis of the expression, prognosis, and immune infiltrates for CHDs in human lung cancer.Discover oncology · 2022Article
- The CHARGE syndrome ortholog CHD-7 regulates TGF-β pathways inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Sentinels of chromatin: chromodomain helicase DNA-binding proteins in development and disease.Genes & development · 2021Review
- P-selectin axis plays a key role in microglia immunophenotype and glioblastoma progression.Nature communications · 2021Article
- Chromatin Imbalance as the Vertex Between Fetal Valproate Syndrome and Chromatinopathies.Frontiers in cell and developmental biology · 2021Review
- Semaphorin Regulation by the Chromatin Remodeler CHD7: An Emerging Genetic Interaction Shaping Neural Cells and Neural Crest in Development and Cancer.Frontiers in cell and developmental biology · 2021Review
- AN1-type zinc finger protein 3 (ZFAND3) is a transcriptional regulator that drives Glioblastoma invasion.Nature communications · 2020Article
- The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer.Cancers · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Chromatin remodeler proteins exert an important function in promoting dynamic modifications in the chromatin architecture, performing a central role in regulating gene transcription. Deregulation of these molecular machines may lead to striking perturbations in normal cell function. The CHD7 gene is a member of the chromodomain helicase DNA-binding family and, when mutated, has been shown to be the cause of the CHARGE syndrome, a severe developmental human disorder. Moreover, CHD7 has been described to be essential for neural stem cells and it is also highly expressed or mutated in a number of human cancers. However, its potential role in glioblastoma has not yet been tested. Here, we show that CHD7 is up-regulated in human glioma tissues and we demonstrate that CHD7 knockout (KO) in LN-229 glioblastoma cells suppresses anchorage-independent growth and spheroid invasion in vitro. Additionally, CHD7 KO impairs tumor growth and increases overall survival in an orthotopic mouse xenograft model. Conversely, ectopic overexpression of CHD7 in LN-428 and A172 glioblastoma cell lines increases cell motility and invasiveness in vitro and promotes LN-428 tumor growth in vivo. Finally, RNA-seq analysis revealed that CHD7 modulates a specific transcriptional signature of invasion-related target genes. Further studies should explore clinical-translational implications for glioblastoma treatment.
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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.