ArticleCell cycle (Georgetown, Tex.)2013
Caveolin-1 is a negative regulator of tumor growth in glioblastoma and modulates chemosensitivity to temozolomide.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- BRAT1 - a new therapeutic target for glioblastoma.Cellular and molecular life sciences : CMLS · 2025Article
- The role of imprinting genes' loss of imprints in cancers and their clinical implications.Frontiers in oncology · 2024Review
- Caveolin-1 promotes tumor cell proliferation and vasculogenic mimicry formation in human glioma.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- Article
- Surfaceome Proteomic of Glioblastoma Revealed Potential Targets for Immunotherapy.Frontiers in immunology · 2021Article
- Caveolin-1, a Key Mediator Across Multiple Pathways in Glioblastoma and an Independent Negative Biomarker of Patient Survival.Frontiers in oncology · 2021Article
- Deregulated expression of the imprinted DLK1-DIO3 region in glioblastoma stemlike cells: tumor suppressor role of lncRNA MEG3.Neuro-oncology · 2020Article
- Article
- Caveolin-1, a master regulator of cellular senescence.Cancer metastasis reviews · 2020Review
- Investigation of Inter- and Intratumoral Heterogeneity of Glioblastoma Using TOF-SIMS.Molecular & cellular proteomics : MCP · 2020Article
- Integrated analysis identified core signal pathways and hypoxic characteristics of human glioblastoma.Journal of cellular and molecular medicine · 2019Article
- The role of caveolin-1 in tumors of the brain - functional and clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- Cell Intrinsic and Extrinsic Mechanisms of Caveolin-1-Enhanced Metastasis.Biomolecules · 2019Review
- Exosomal transfer of miR-1238 contributes to temozolomide-resistance in glioblastoma.EBioMedicine · 2019Article
- ANLN and KDR Are Jointly Prognostic of Breast Cancer Survival and Can Be Modulated for Triple Negative Breast Cancer Control.Frontiers in genetics · 2019Article
- Caveolin-1-Knockout Mouse as a Model of Inflammatory Diseases.Journal of immunology research · 2018Article
- Article
- Galectin-3 induces ovarian cancer cell survival and chemoresistance via TLR4 signaling activation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- ∆Np73beta induces caveolin-1 in human non-small cell lung cancer cell line H1299.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Microarray Analysis in Glioblastomas.Methods in molecular biology (Clifton, N.J.) · 2016Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolin-1 (Cav-1) is a critical regulator of tumor progression in a variety of cancers where it has been shown to act as either a tumor suppressor or tumor promoter. In glioblastoma multiforme, it has been previously demonstrated to function as a putative tumor suppressor. Our studies here, using the human glioblastoma-derived cell line U-87MG, further support the role of Cav-1 as a negative regulator of tumor growth. Using a lentiviral transduction approach, we were able to stably overexpress Cav-1 in U-87MG cells. Gene expression microarray analyses demonstrated significant enrichment in gene signatures corresponding to downregulation of MAPK, PI3K/AKT and mTOR signaling, as well as activation of apoptotic pathways in Cav-1-overexpressing U-87MG cells. These same gene signatures were later confirmed at the protein level in vitro. To explore the ability of Cav-1 to regulate tumor growth in vivo, we further show that Cav-1-overexpressing U-87MG cells display reduced tumorigenicity in an ectopic xenograft mouse model, with marked hypoactivation of MAPK and PI3K/mTOR pathways. Finally, we demonstrate that Cav-1 overexpression confers sensitivity to the most commonly used chemotherapy for glioblastoma, temozolomide. In conclusion, Cav-1 negatively regulates key cell growth and survival pathways and may be an effective biomarker for predicting response to chemotherapy in glioblastoma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.