ArticleDiscover oncology2025
Aberrant expression of CNTRL was associated with poor prognosis, immune response and progression in glioma.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study investigated the biological functions and prognostic significance of centromere protein L (CNTRL) in glioma. mRNA expression data and clinical information were obtained from TCGA, CGGA, and an independent cohort of 207 glioma patients. CNTRL expression levels were quantified using qRT-PCR. Functional analyses, including Gene Ontology and KEGG pathway enrichment, were conducted to elucidate the biological roles of CNTRL. Kaplan-Meier survival curves and Cox regression analyses were applied to evaluate its association with overall survival, and a nomogram was constructed to predict individual survival. Additionally, the tumor microenvironment and immune cell infiltration were analyzed. Glioma cell lines were transfected with CNTRL-targeting shRNA to explore its functional role in cell proliferation, migration, and invasion, utilizing CCK-8, colony formation, scratchy and Transwell assays. The results revealed that CNTRL is ubiquitously expressed in brain tissues and is significantly upregulated in glioma. Higher CNTRL expression was positively correlated with increased tumor grade and were associated with poor prognosis in glioma patients. Furthermore, univariate and multivariate Cox regression analyses identified CNTRL as an independent prognostic factor for glioma survival. The nomogram model integrating CNTRL expression and clinical parameters demonstrated robust predictive performance for patient survival. Functional enrichment analyses suggested that CNTRL is involved in key cellular processes such as cell cycle, DNA repair, and chromatin remodeling. CNTRL expression was positively associated with enhanced immune cell infiltration and activation within the tumor microenvironment, as well as with the expression of immune checkpoint molecules, implicating its potential role in immune evasion mechanisms. In vitro, CNTRL knockdown significantly inhibited glioma cell proliferation, migration, and invasion. Notably, suppression of CNTRL led to reduced expression of the cell cycle regulator WEE1 in glioma cells. This study provides comprehensive evidence that CNTRL contributes to glioma progression by regulating the cell cycle and immune-related processes. Targeting CNTRL could represent a promising therapeutic strategy for glioma. These findings underscore the potential of CNTRL as a prognostic biomarker and a therapeutic target in glioma management.
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