ArticleHeliyon2024
Caveolin-1 promotes glioma proliferation and metastasis by enhancing EMT via mediating PAI-1 activation and its correlation with immune infiltrates.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- ARNTL2 promotes metastatic phenotypes through SERPINE1 transcription in KRAS G12D pancreatic cancer.iScience · 2026Article
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- Identification of a Two-Gene Biomarker Correlated with Sensitivity to Combined PARP7 Inhibition and AHR Activation in Cancer Cells.Cancer research communications · 2026Article
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- Proteomic Analysis Uncovers Enhanced Inflammatory Phenotype and Distinct Metabolic Changes in IDH1 Mutant Glioma Cells.International journal of molecular sciences · 2025Article
- Application of the Mass Spectrometry-High-Throughput Technique Over the Immunohistochemical Analysis for Human Brain Tumor Diagnosis and Prognosis: Insights Into Biomarkers' Identification for the Case Study of Grade IV Astrocytomas and Meningiomas.Biomedical chromatography : BMC · 2025Article
- Targeting autophagy and plasminogen activator inhibitor-1 increases survival and remodels the tumor microenvironment in glioblastoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Caveolae: Metabolic Platforms at the Crossroads of Health and Disease.International journal of molecular sciences · 2025Review
- Huafengdan Inhibits Glioblastoma Cell Growth and Mobility by Acting on PLAU and CAV1 Targets.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Molecular Mechanisms of Neutrophil Extracellular Traps in Promoting Gastric Cancer Epithelial-Mesenchymal Transition Through SERPINE-1 Expression.Journal of biochemical and molecular toxicology · 2025Article
- Constructing a Glioblastoma Prognostic Model Related to Fatty Acid Metabolism Using Machine Learning and Identifying F13A1 as a Potential Target.Biomedicines · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma is typically characterized by a poor prognosis and is associated with a decline in the quality of life as the disease advances. However, the development of effective therapies for glioma has been inadequate. Caveolin-1 (CAV-1) is a membrane protein that plays a role in caveolae formation and interacts with numerous signaling proteins, compartmentalizing them in caveolae and frequently exerting direct control over their activity through binding to its scaffolding domain. Although CAV-1 is a vital regulator of tumour progression, its role in glioma remains unclear. Our findings indicated that the knockdown of CAV-1 significantly inhibits the proliferation and metastasis of glioma. Subsequent mechanistic investigations demonstrated that CAV-1 promotes proliferation and metastasis by activating the photoshatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Furthermore, we demonstrated that CAV-1 overexpression upregulates the expression of serpin peptidase inhibitor, class E, member 1 (SERPINE1, also known as PAI-1), which serves as a marker for the epithelial-mesenchymal transition (EMT) process. Further research showed that PAI-1 knockdown abolished the CAV-1 mediated activation of PI3K/Akt signaling pathway. In glioma tissues, CAV-1 expression exhibited a correlation with unfavorable prognosis and immune infiltration among glioma patients. In summary, our study provided evidence that CAV-1 activates the PI3K/Akt signaling pathway by upregulating PAI-1, thereby promoting the proliferation and metastasis of glioma through enhanced epithelial-mesenchymal transition (EMT) and angiogenesis, and CAV-1 is involved in the immune infiltration.
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