ArticlePloS one2024
High Caveolin-1 mRNA expression in triple-negative breast cancer is associated with an aggressive tumor microenvironment, chemoresistance, and poor clinical outcome.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- What is the Impact of Endothelial-to-Mesenchymal Transition in Solid Tumours: A Qualitative Systematic Review and Quantitative Meta-Analysis.International journal of biological sciences · 2025Pooled it
- Predictive value of serial dynamic lipid monitoring for pathologic complete response to neoadjuvant chemotherapy in luminal breast cancer: a retrospective study integrating metabolic and clinical indicators.BMC women's health · 2026Article
- Caveolin-1 drives immunosuppression in esophageal squamous cell carcinoma by enhancing exosome secretion and macrophage M2 polarization via inhibition of MVB autophagic degradation.Journal of translational medicine · 2026Article
- The progression of triple-negative breast cancer is linked to a gradual decrease of the BK channel in the plasma membrane and an increase in intracellular structures.Pflugers Archiv : European journal of physiology · 2026Article
- Microenvironment Modulates Tumorigenicity of Breast Cancer Cells Depending on Hormone Receptor Status.International journal of molecular sciences · 2026Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCurrently, there are few treatment-predictive and prognostic biomarkers in triple-negative breast cancer (TNBC). Caveolin-1 (CAV1) is linked to chemoresistance and several important processes involved in tumor progression and metastasis, such as epithelial-mesenchymal transition (EMT). Herein, we report that high CAV1 gene expression is an independent factor of poor prognosis in TNBC.
methodsCAV1 gene expression was compared across different molecular features (e.g., PAM50 subtypes). CAV1 expression was assessed in relation to clinical outcomes using Cox regression adjusted for clinicopathological predictors. Differential gene expression and gene set enrichment analyses were applied to compare high- and low-expressing CAV1 tumors. Tumor microenvironment composition of high- and low-expressing CAV1 tumors was estimated using ECOTYPER. Tumor tissue microarrays were used to evaluate CAV1 protein levels in stromal and malignant cells.
resultsIn the SCAN-B (n = 525) and GSE31519 (n = 327) cohorts, patients with CAV1-high tumors had an increased incidence of early recurrence adjusted HR 1.78 (95% CI 1.12-2.81) and 2.20 (95% CI 1.39-3.47), respectively. In further analysis, high CAV1 gene expression was associated with a molecular profile indicating altered metabolism, neovascularization, chemoresistance, EMT, suppressed immune response, and active tumor microenvironment. Protein levels of CAV1 in malignant and stromal cells were not correlated with CAV1 gene expression.
conclusionCAV1 gene expression in TNBC is a biomarker that merits further investigation in clinical trials and as a therapeutic target.
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