ArticleCell death & disease2020
Caveolin-1 inhibits breast cancer stem cells via c-Myc-mediated metabolic reprogramming.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 63 citations in OpenAlex.
- Caveolae in cancer: mechanochemical signaling in tumor progression, immunity, and therapy.Cell communication and signaling : CCS · 2026Review
- Review
- Decoding the Role of Caveolin-1 in Morphological Diversity and Self-Renewal of Breast Cancer Cells.Cell proliferation · 2026Article
- Therapeutic role of caveolin family in stem cell fate and development for management of chronic degenerative diseases: A scientometric study to an in-depth review.Journal of advanced research · 2026Review
- Article
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- Navigating the therapeutic landscape for breast cancer: targeting breast cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- CAV1 inhibits XcTranslational oncology · 2024Article
- Tumor-associated macrophages/C-X-C motif chemokine ligand 1 promotes breast cancer autophagy-mediated chemoresistance via IGF1R/STAT3/HMGB1 signaling.Cell death & disease · 2024Article
- Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.Journal of experimental & clinical cancer research : CR · 2024Article
- Caveolin-1 gene expression provides additional prognostic information combined with PAM50 risk of recurrence (ROR) score in breast cancer.Scientific reports · 2024Article
- Trafficking in cancer: from gene deregulation to altered organelles and emerging biophysical properties.Frontiers in cell and developmental biology · 2024Review
- Article
- MicroRNA-142-3p chemo-sensitizing breast cancer to docetaxel: apoptosis and cell cycle arrest induction, and migration suppression.Veterinary research forum : an international quarterly journal · 2024Article
- Caveolin-1, a Determinant of the Fate of MCF-7 Breast Cancer Cells.Breast cancer : basic and clinical research · 2024Article
- Caveolin-1 mediates the utilization of extracellular proteins for survival in refractory gastric cancer.Experimental & molecular medicine · 2023Article
- Role of m6A modification in regulating the PI3K/AKT signaling pathway in cancer.Journal of translational medicine · 2023Review
- A Combined Western and Bead-Based Multiplex Platform to Characterize Extracellular Vesicles.Tissue engineering. Part C, Methods · 2023Article
- The Ubiquitin-Proteasome System in Tumor Metabolism.Cancers · 2023Review
- Role of Caveolae family-related proteins in the development of breast cancer.Frontiers in molecular biosciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer stem cells (BCSCs) are considered to be the root of breast cancer occurrence and progression. However, the characteristics and regulatory mechanisms of BCSCs metabolism have been poorly revealed, which hinders the development of metabolism-targeted treatment strategies for BCSCs elimination. Herein, we demonstrated that the downregulation of Caveolin-1 (Cav-1) usually occurred in BCSCs and was associated with a metabolic switch from mitochondrial respiration to aerobic glycolysis. Meanwhile, Cav-1 could inhibit the self-renewal capacity and aerobic glycolysis activity of BCSCs. Furthermore, Cav-1 loss was associated with accelerated mammary-ductal hyperplasia and mammary-tumor formation in transgenic mice, which was accompanied by enrichment and enhanced aerobic glycolysis activity of BCSCs. Mechanistically, Cav-1 could promote Von Hippel-Lindau (VHL)-mediated ubiquitination and degradation of c-Myc in BCSCs through the proteasome pathway. Notably, epithelial Cav-1 expression significantly correlated with a better overall survival and delayed onset age of breast cancer patients. Together, our work uncovers the characteristics and regulatory mechanisms of BCSCs metabolism and highlights Cav-1-targeted treatments as a promising strategy for BCSCs elimination.
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Registered trials
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.