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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 7454031, 20 pages
Review Article

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

1Department of Mammary Disease, Discipline of Integrated Chinese and Western Medicine in Guangzhou University of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
2The Research Center for Integrative Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
3Post-Doctoral Research Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
4Department of Breast Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China

Correspondence should be addressed to Zhiyu Wang; moc.621@679uyihzgnaw

Received 6 November 2016; Revised 23 January 2017; Accepted 7 March 2017; Published 4 May 2017

Academic Editor: Ilaria Peluso

Copyright © 2017 Shengqi Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.