Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention

Abstract

Aberrant oxidative metabolism is one of the hallmarks of cancer. Reactive species overproduction could promote carcinogenesis via inducing genetic mutations and activating oncogenic pathways, and thus, antioxidant therapy was considered as an important strategy for cancer prevention and treatment. Caveolin-1 (Cav-1), a constituent protein of caveolae, has been shown to mediate tumorigenesis and progression through oxidative stress modulation recently. Reactive species could modulate the expression, degradation, posttranslational modifications, and membrane trafficking of Cav-1, while Cav-1-targeted treatments could scavenge the reactive species. More importantly, emerging evidences have indicated that multiple antioxidants could exert antitumor activities in cancer cells and protective activities in normal cells by modulating the Cav-1 pathway. Altogether, these findings indicate that Cav-1 may be a promising oxidative stress-related target for cancer antioxidant prevention. Elucidating the underlying interaction mechanisms between oxidative stress and Cav-1 is helpful for enhancing the preventive effects of antioxidants on cancer, for improving clinical outcomes of antioxidant-related therapeutics in cancer patients, and for developing Cav-1 targeted drugs. Herein, we summarize the available evidence of the roles of Cav-1 and oxidative stress in tumorigenesis and development and shed novel light on designing strategies for cancer prevention or treatment by utilizing the interaction mode between Cav-1 and oxidative stress.

MicroRNA‑124 inhibits cell proliferation, invasion and migration by targeting CAV1 in bladder cancer

“…Increased expression of CAV1 was observed in high-grade BC, and CAV1 has been suggested to be a potential target for cancer prevention (22–24). However, the regulatory mechanism of CAV1 expression in BC remains elusive.…”

Caveolin‐1, cancer and therapy resistance

“…140 Thus, restoring CAV1 expression in respective stromal cells could inhibit the cancer cell metabolism. [141][142][143] Excessive reactive species not only induce oxidative damages and inactivation of tumor suppressor genes but also activate the phosphorylation of CAV1, which was reported to promote cancer cell growth and survival. 143,144 Conclusively, targeting CAV1 and the associated metabolism may be a more promising therapeutic strategy for eliminating cancer cells.…”

“…[141][142][143] Excessive reactive species not only induce oxidative damages and inactivation of tumor suppressor genes but also activate the phosphorylation of CAV1, which was reported to promote cancer cell growth and survival. 143,144 Conclusively, targeting CAV1 and the associated metabolism may be a more promising therapeutic strategy for eliminating cancer cells. 143 Another resistance promoting factor is autophagy, as cancers can upregulate autophagy to survive microenvironmental stress and to increase growth and aggressiveness.…”

“…143,144 Conclusively, targeting CAV1 and the associated metabolism may be a more promising therapeutic strategy for eliminating cancer cells. 143 Another resistance promoting factor is autophagy, as cancers can upregulate autophagy to survive microenvironmental stress and to increase growth and aggressiveness. 145 CAV1 was already directly associated with autophagy.…”

“…TP53‐induced glycolysis and apoptosis regulator was further upregulated in the co‐cultured breast cancer cells, which resulted in apoptosis inhibition, and thus supports the hypothesis that stromal CAV1 possesses tumor‐suppressor properties, whereas loss of stromal CAV1 fosters malignant epithelial cell resistance by evading apoptosis . Thus, restoring CAV1 expression in respective stromal cells could inhibit the cancer cell metabolism . Excessive reactive species not only induce oxidative damages and inactivation of tumor suppressor genes but also activate the phosphorylation of CAV1, which was reported to promote cancer cell growth and survival .…”