ArticleOncotarget2016
Caveolin-1 regulates cancer cell metabolism via scavenging Nrf2 and suppressing MnSOD-driven glycolysis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- TKT regulates the pentose phosphate pathway via RBKS to promote epithelial-mesenchymal transition during AML progression.Journal of bioenergetics and biomembranes · 2025Article
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- Inhibition of CAV1 attenuates diabetic cardiomyopathy through reducing ferroptosis via activating NRF2/GCLC signaling pathway.Theranostics · 2025Article
- JFD, a Novel Natural Inhibitor of Keap1 Alkylation, Suppresses IntracellularOxidative medicine and cellular longevity · 2023Article
- Nrf2 Modulation in Breast Cancer.Biomedicines · 2022Review
- The genomic response of human granulosa cells (KGN) to melatonin and specific agonists/antagonists to the melatonin receptors.Scientific reports · 2022Article
- HuR-dependent SOD2 protein synthesis is an early adaptation to anchorage-independence.Redox biology · 2022Article
- Caveolin-1 controls mitochondrial damage and ROS production by regulating fission - fusion dynamics and mitophagy.Redox biology · 2022Article
- Review
- Targeting prooxidant MnSOD effect inhibits triple-negative breast cancer (TNBC) progression and M2 macrophage functions under the oncogenic stress.Cell death & disease · 2022Article
- TKTL1 participated in malignant progression of cervical cancer cells via regulating AKT signal mediated PFKFB3 and thus regulating glycolysis.Cancer cell international · 2021Article
- Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension.Medical sciences (Basel, Switzerland) · 2021Review
- Involvement of NRF2 in Breast Cancer and Possible Therapeutical Role of Polyphenols and Melatonin.Molecules (Basel, Switzerland) · 2021Review
- Expression of Autophagy and Mitophagy Markers in Breast Cancer Tissues.Frontiers in oncology · 2021Article
- Inorganic arsenic promotes luminal to basal transition and metastasis of breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The NRF2, Thioredoxin, and Glutathione System in Tumorigenesis and Anticancer Therapies.Antioxidants (Basel, Switzerland) · 2020Review
- Nuclear Factor Erythroid 2-Related Factor 2 in Regulating Cancer Metabolism.Antioxidants & redox signaling · 2020Review
- NRF2 and PPAR-γ Pathways in Oligodendrocyte Progenitors: Focus on ROS Protection, Mitochondrial Biogenesis and Promotion of Cell Differentiation.International journal of molecular sciences · 2020Article
- Article
- Caveolin-1 inhibits breast cancer stem cells via c-Myc-mediated metabolic reprogramming.Cell death & disease · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Aerobic glycolysis is an indispensable component of aggressive cancer cell metabolism. It also distinguishes cancer cells from most healthy cell types in the body. Particularly for this reason, targeting the metabolism to improve treatment outcomes has long been perceived as a potentially valuable strategy. In practice, however, our limited knowledge of why and how metabolic reprogramming occurs has prevented progress towards therapeutic interventions that exploit the metabolic peculiarities of tumors. We recently described that in breast cancer, MnSOD upregulation is both necessary and sufficient to activate glycolysis. Here, we focused on determining the molecular mechanisms of MnSOD upregulation. We found that Caveolin-1 (Cav-1) is a central component of this mechanism due to its suppressive effects of NF-E2-related factor 2 (Nrf2), a transcription factor upstream of MnSOD. In transformed MCF10A(Er/Src) cells, Cav-1 loss preceded the activation of Nrf2 and its induction of MnSOD expression. Consistently, with previous observations, MnSOD expression secondary to Nrf2 activation led to an increase in the glycolytic rate dependent on mtH2O2 production and the activation of AMPK. Moreover, rescue of Cav-1 expression in a breast cancer cell line (MCF7) suppressed Nrf2 and reduced MnSOD expression. Experimental data were reinforced by epidemiologic nested case-control studies showing that Cav-1 and MnSOD are inversely expressed in cases of invasive ductal carcinoma, with low Cav-1 and high MnSOD expression being associated with lower 5-year survival rates and molecular subtypes with poorest prognosis.
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