Caveolin-1, a stress-related oncotarget, in drug resistance

Zhiyu Wang _, Neng Wang, Pengxi Liu, Fu Peng, Hailin Tang, Qianjun Chen, Rui Xu, Yan Dai, Yi Lin, Xiaoming Xie, Cheng Peng and Honglin Situ

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Oncotarget. 2015; 6:37135-37150. https://doi.org/10.18632/oncotarget.5789

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Zhiyu Wang1, Neng Wang2, Pengxi Liu1, Fu Peng3, Hailin Tang2, Qianjun Chen1, Rui Xu1, Yan Dai1, Yi Lin1, Xiaoming Xie2, Cheng Peng3 and Honglin Situ1

1 Department of Mammary Disease, Guangdong Provincial Hospital of Chinese Medicine, The Second Clinical Collage of Guangzhou University of Chinese Medicine, Guangzhou, China

2 Department of Breast Oncology, Sun Yat-sen Univeristy Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China

3 Pharmacy College, State Key Laboratory Breeding Base of Systematic Research, Development and Utilization of Chinese Medicine Resources, Chengdu University of Traditional Chinese Medicine, Guangzhou, China

Correspondence to:

Zhiyu Wang, email:

Keywords: Cav-1, cancer drug resistance, aerobic glycolysis, cancer stem cells, ABC transporters

Received: May 19, 2015 Accepted: September 08, 2015 Published: September 27, 2015


Caveolin-1 (Cav-1) is both a tumor suppressor and an oncoprotein. Cav-1 overexpression was frequently confirmed in advanced cancer stages and positively associated with ABC transporters, cancer stem cell populations, aerobic glycolysis activity and autophagy. Cav-1 was tied to various stresses including radiotherapy, fluid shear and oxidative stresses and ultraviolet exposure, and interacted with stress signals such as AMP-activated protein kinase. Finally, a Cav-1 fluctuation model during cancer development is provided and Cav-1 is suggested to be a stress signal and cytoprotective. Loss of Cav-1 may increase susceptibility to oncogenic events. However, research to explore the underlying molecular network between Cav-1 and stress signals is warranted.

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