Proteomics-based identification of VDAC1 as a tumor promoter in cervical carcinoma
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Changlin Zhang1,2,*, Wencheng Ding1,*, Yuan Liu3, Zheng Hu1, Da Zhu1, Xiaoli Wang1, Lan Yu1, Liming Wang1, Hui Shen1, Weican Zhang4, Ci Ren1, Kezhen Li1, Danhui Weng1, Wuguo Deng2, Ding Ma1, Hui Wang1
1Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
2Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, Guangdong 510060, China
3The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Sichuan 610041, China
4Department of Obstetrics and Gynecology, Hebei Medical University, Shijiazhuang, Hebei 050017, China
*These authors contributed equally to this work
Hui Wang, email: [email protected]
Ding Ma, email: [email protected]
Keywords: proteomics, immunohistochemistry (IHC), cervical cancer, VDAC1, HPV16 E7
Received: November 04, 2015 Accepted: June 12, 2016 Published: July 13, 2016
We used oxidative isotope-coded affinity tags (OxICAT) to investigate the global redox status of proteins in human papillomavirus (HPV)-related cervical cancer cells, in order to identify a potential target for gene therapy. Voltage-dependent anion channel 1 (VDAC1) was found to be highly oxidized in HPV-positive cervical cancer cells. VDAC1 expression correlated significantly with the invasion of cervical cancer, the grade of cervical intraepithelial neoplasia (CIN) and the expression of HPV16 E7 in CIN. Knockdown of VDAC1 in cell lines increased the rate of apoptosis, while overexpression of the VDAC1 (respectively) partly reversed the effect. Thus, VDAC1 may promote the malignant progression of HPV-related disease, and treatments designed to suppress VDAC1 could prevent the progression of HPV-induced cervical disease.
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