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Updated: Jul 17, 2025

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
Published on: July 31, 2017
Caveolin-1 promotes glioma progression and maintains its mitochondrial inhibition resistance
Yu'e Liu1, Yi Chen2, Fei Wang3
1Department of Neurosurgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Background:
Glioma is a lethal brain cancer and lacking effective therapies. Challenges include no effective therapeutic target, intra- and intertumoral heterogeneity, inadequate effective drugs, and an immunosuppressive microenvironment, etc. Deciphering the pathogenesis of gliomas and finding out the working mechanisms are urgent and necessary for glioma treatment. Identification of prognostic biomarkers and targeting the biomarker genes will be a promising therapy.
Methods:
From our RNA-sequencing data of the oxidative phosphorylation (OXPHOS)-inhibition sensitive and OXPHOS-resistant cell lines, we found that the scaffolding protein caveolin 1 (CAV1) is highly expressed in the resistant group but not in the sensitive group. By comprehensive analysis of our RNA sequencing data, Whole Genome Bisulfite Sequencing (WGBS) data and public databases, we found that CAV1 is highly expressed in gliomas and its expression is positively related with pathological processes, higher CAV1 predicts shorter overall survival.
Results:
Further analysis indicated that (1) the differentiated genes in CAV1-high groups are enriched in immune infiltration and immune response; (2) CAV1 is positively correlated with tumor metastasis markers; (3) the methylation level of CAV1 promoters in glioma group is lower in higher stage than that in lower stage; (4) CAV1 is positively correlated with glioma stemness; (5) higher expression of CAV1 renders the glioma cells' resistant to oxidative phosphorylation inhibitors.
Conclusion:
Therefore, we identified a key gene CAV1 and deciphered its function in glioma progression and prognosis, proposing that CAV1 may be a therapeutic target for gliomas.
Insights
Caveolin 1 (CAV1) is highly expressed in aggressive gliomas, promoting tumor growth, metastasis, and resistance to therapy. Targeting CAV1 offers a promising therapeutic strategy for this lethal brain cancer.
Area of Science:
- Neuro-oncology
- Cancer Biology
- Molecular Medicine
Background:
- Glioma is a fatal brain cancer with limited therapeutic options due to challenges like heterogeneity and an immunosuppressive microenvironment.
- Identifying novel therapeutic targets and understanding glioma pathogenesis are critical for improving patient outcomes.
- Prognostic biomarkers are essential for guiding treatment strategies in glioma patients.
Purpose of the Study:
- To investigate the role of scaffolding protein caveolin 1 (CAV1) in glioma progression and its potential as a therapeutic target.
- To analyze the correlation between CAV1 expression and glioma characteristics, including resistance to oxidative phosphorylation inhibitors.
Main Methods:
- RNA-sequencing of oxidative phosphorylation (OXPHOS)-inhibition sensitive and resistant glioma cell lines.
- Comprehensive analysis of RNA sequencing, Whole Genome Bisulfite Sequencing (WGBS) data, and public databases.
- Correlation analysis of CAV1 expression with pathological processes, immune infiltration, metastasis, stemness, and patient survival.
Main Results:
- CAV1 is highly expressed in OXPHOS-resistant glioma cells and gliomas, with higher expression correlating with poorer overall survival.
- CAV1 expression is linked to immune infiltration, tumor metastasis, and glioma stemness.
- Lower CAV1 promoter methylation was observed in higher-stage gliomas, and high CAV1 expression conferred resistance to OXPHOS inhibitors.
Conclusions:
- Caveolin 1 (CAV1) is identified as a key gene in glioma progression, influencing multiple pathological processes.
- CAV1 promotes glioma aggressiveness, metastasis, and therapeutic resistance.
- CAV1 represents a potential therapeutic target for improving glioma treatment outcomes.
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