ArticleFrontiers in immunology2025
Molecular insights into glioblastoma progression: role of CHCHD2P9 in tumor heterogeneity and prognosis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Retraction Note: Methylation-induced suppression of BEX1 activates AKT/ERK/STAT3 signaling pathways regulating cell cycle and apoptosis in glioma.Scientific reports · 2026Article
- GFAP-Dependent Transcriptional Dynamics and Cellular Heterogeneity in Primary, Recurrent, and Grade III Gliomas.Cancer informatics · 2026Article
- Dissecting tumor heterogeneity in colorectal cancer: uncovering the role of BCL2L1Frontiers in immunology · 2026Article
- Single-cell multi-omics dissection of c-Myb/AURKA-mediated autophagy and metabolic reprogramming in diabetic adipose-derived stem cells.Frontiers in immunology · 2025Article
- Deciphering oligomeric proanthocyanidins' dual osteoprotective mechanisms at single-cell resolution:Frontiers in immunology · 2025Article
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Authors and funding
12 authors.
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Abstract
Background: Gliomas are highly aggressive, life-threatening tumors with poor prognosis, and remain a leading cause of mortality among brain cancers. Although the role of mitochondrial proteins in cancer has garnered increasing attention, their specific functions in the nervous system, particularly in gliomas, remain poorly understood. Methods: We integrated single-cell RNA sequencing with cellular assays and flow cytometry to investigate the molecular characteristics and cellular interactions within glioblastoma subpopulations during tumor progression. Results: Single-cell RNA sequencing revealed several differentially expressed genes (DEGs) within glioblastoma subpopulations. Trajectory analysis identified CHCHD2P9 as a pivotal marker for the terminal subpopulation. Moreover, elevated expression of CHCHD2P9 was found to correlate with poorer clinical outcomes. Subsequent cellular experiments further explored the underlying mechanisms driving these observations. Conclusions: CHCHD2P9 is significantly overexpressed in glioma patients, and its differential expression plays a crucial role in regulating glioma cell proliferation and migration. A CHCHD2P9-based risk model holds promise as both a prognostic biomarker and a potential therapeutic target, providing novel insights into the pathogenesis of gliomas and opening avenues for personalized treatment strategies.
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