ArticleBritish journal of cancer2020
Defining COMMD4 as an anti-cancer therapeutic target and prognostic factor in non-small cell lung cancer.
Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring the promise of regulator of G Protein Signaling 20: insights into potential mechanisms and prospects across solid cancers and hematological malignancies.Cancer cell international · 2024Review
- Article
- COMMD10 inhibited DNA damage to promote the progression of gastric cancer.Journal of cancer research and clinical oncology · 2024Article
- Copper metabolism and cuproptosis in human malignancies: Unraveling the complex interplay for therapeutic insights.Heliyon · 2024Review
- Decoding Gastric Cancer: Machine Learning Insights Into the Significance of COMMDs Family in Immunotherapy and Diagnosis.Journal of Cancer · 2024Article
- Targeting the COMMD4-H2B protein complex in lung cancer.British journal of cancer · 2023Article
- Multi-omics analysis of the oncogenic value of copper Metabolism-Related protein COMMD2 in human cancers.Cancer medicine · 2023Article
- COMMD proteins function and their regulating roles in tumors.Frontiers in oncology · 2023Review
- Identification of copper metabolism-related subtypes and establishment of the prognostic model in ovarian cancer.Frontiers in endocrinology · 2023Article
- Inhibitory effects of total triterpenoids isolated from theFrontiers in pharmacology · 2022Article
- COMMD4 is a novel prognostic biomarker and relates to potential drug resistance mechanism in glioma.Frontiers in pharmacology · 2022Article
- Transcriptional analysis of the expression, prognostic value and immune infiltration activities of the COMMD protein family in hepatocellular carcinoma.BMC cancer · 2021Article
- COMMD4 functions with the histone H2A-H2B dimer for the timely repair of DNA double-strand breaks.Communications biology · 2021Article
- COMMD1, from the Repair of DNA Double Strand Breaks, to a Novel Anti-Cancer Therapeutic Target.Cancers · 2021Article
- Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review.Frontiers in molecular biosciences · 2021Review
- Cytoplasmic Localization Isoform of Cyclin Y Enhanced the Metastatic Ability of Lung CancerFrontiers in cell and developmental biology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNon-small cell lung cancers (NSCLC) account for 85-90% of all lung cancers. As drug resistance critically impairs chemotherapy effectiveness, there is great need to identify new therapeutic targets. The aims of this study were to investigate the prognostic and therapeutic potential of the copper-metabolism-domain-protein, COMMD4, in NSCLC.
methodsThe expression of COMMD4 in NSCLC was investigated using bioinformatic analysis, immunoblotting of immortalised human bronchial epithelial (HBEC) and NSCLC cell lines, qRT-PCR and immunohistochemistry of tissue microarrays. COMMD4 function was additionally investigated in HBEC and NSCLC cells depleted of COMMD4, using small interfering RNA sequences.
resultsBioinformatic analysis and in vitro analysis of COMMD4 transcripts showed that COMMD4 levels were upregulated in NSCLC and elevated COMMD4 was associated with poor prognosis in adenocarcinoma (ADC). Immunoblotting demonstrated that COMMD4 expression was upregulated in NSCLC cells and siRNA-depletion of COMMD4, decreased cell proliferation and reduced cell viability. Cell death was further enhanced after exposure to DNA damaging agents. COMMD4 depletion caused NSCLC cells to undergo mitotic catastrophe and apoptosis.
conclusionsOur data indicate that COMMD4 may function as a prognostic factor in ADC NSCLC. Additionally, COMMD4 is a potential therapeutic target for NSCLC, as its depletion induces cancer cell death.
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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.