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

Figure 3

Cav-1 loss facilitates carcinogenesis through activating NOS activity. Cav-1 could directly interact with NOS enzymes through the scaffolding region. Following Cav-1 loss, eNOS will be released from the complex and activated through phosphorylation and mRNA overexpression, leading to the overproduction of NO and RNS. The high levels of NO and/or RNS would facilitate cell proliferation, apoptosis evasion, angiogenesis, and EMT process and finally induce carcinogenic transformation. Besides eNOS, iNOS will also be activated following Cav-1 loss. Since iNOS is capable of generating the micromolar level of NO, its activation will bring RNS burst and results in DNA damage and mitochondrial dysfunction, which finally promotes carcinogenesis.