ArticleAnnals of translational medicine2022
Bromodomain-containing protein 4 activates cardiotrophin-like cytokine factor 1, an unfavorable prognostic biomarker, and promotes glioblastoma
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Comprehensive Analysis of scRNA-Seq and RNA-Seq Revealed the Role of Programmed Cell Death-Related Genes in the Prognosis of Glioblastoma Patients.Applied biochemistry and biotechnology · 2026Article
- A Prognostic Neuromodulation-Related Gene Signature Identifies Immunomodulation and Tumour-Associated Hallmarks in Glioblastoma.Biomedicines · 2025Article
- Identifying survival subtypes with autoencoder using multiple types of high-dimensional genomic data from studies of glioblastoma multiforme.Briefings in bioinformatics · 2025Article
- A novel immune-related gene prognostic signature combining immune cell infiltration and immune checkpoint for glioblastoma patients.Translational cancer research · 2024Article
- CLCF1 inhibits energy expenditure via suppressing brown fat thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Comprehensive analysis of the prognosis and immune infiltrates for the BET protein family reveals the significance of BRD4 in glioblastoma multiforme.Frontiers in cell and developmental biology · 2023Article
- Overexpression of TMEM150A in glioblastoma multiforme patients correlated with dismal prognoses and compromised immune statuses.PloS one · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioblastoma (GBM) is one of the most common and malignant brain tumors. Cardiotrophin-like cytokine factor 1 (CLCF1) is a member of the IL-6 superfamily. However, the clinical significance, potential role, and molecular mechanism of CLCF1 in GBM remain obscure. Here, the expression and prognostic significance of CLCF1 was investigated in GBM. Methods: The Cancer Genome Atlas (TCGA) GBM and Chinese Glioma Genome Atlas (CGGA) datasets were downloaded and analyzed by using Gene Expression Profiling Interactive Analysis (GEPIA). Next, 3 shRNAs targeting CLCF1 were designed, and silencing efficiency was examined with real-time polymerase chain reaction (PCR). Cell Counting Kit 8 (CCK-8), flow cytometry, transwell, and wound healing assays were used to study the function of CLCF1 in glioma cells. Results: We found increased expression of CLCF1 as an unfavorable prognostic marker in GBM. Functionally, down-regulation of CLCF1 significantly reduced cell proliferation, induced cell apoptosis and cell cycle G2 phase arrest, and weakened the migration and invasion of GBM cells. Downstream pathway analysis was conducted, and potential targets in cytokine receptors, extracellular matrix (ECM) receptors, apoptosis, and the cell cycle were uncovered. Finally, transcriptional regulators were analyzed, and bromodomain-containing protein 4 (BRD4) was found to activate CLCF1 in GBM. Conclusions: CLCF1, transcriptionally activated by BRD4, promotes glioma and serves as an unfavorable marker in GBM.
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