Identification and validation of differentially expressed proteins in epithelial ovarian cancers using quantitative proteomics
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Hong Qu1,*, Yuling Chen2,3,*, Guangming Cao1, Chongdong Liu1, Jiatong Xu3, Haiteng Deng3, Zhenyu Zhang1
1Department of Obstetrics & Gynecology, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing, China
2Tsinghua University-Peking University Joint Center for Life Sciences, Beijing, China
3MOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing, China
*These authors have contributed equally to this work
Zhenyu Zhang, email: [email protected]
Haiteng Deng, email: [email protected]
Keywords: proteomics, epithelial ovarian cancer, CLIC1, LGALS3BP, therapeutic target
Received: May 02, 2016 Accepted: October 19, 2016 Published: November 4, 2016
Ovarian cancer is the most lethal gynecological malignant tumor because of its high recurrence rate. In the present work, in order to find new therapeutic targets, we identified 8480 proteins in thirteen pairs of ovarian cancer tissues and normal ovary tissues through quantitative proteomics. 498 proteins were found to be differentially expressed in ovarian cancer, which involved in various cellular processes, including metabolism, response to stimulus and biosynthetic process. The expression levels of chloride intracellular channel protein 1 (CLIC1) and lectin galactoside-binding soluble 3 binding protein (LGALS3BP) in epithelial ovarian cancer tissues were significantly higher than those in normal ovary tissues as confirmed by western blotting and immunohistochemistry. The knockdown of CLIC1 in A2780 cell line downregulated expression of CTPS1, leading to the decrease of CTP and an arrest of cell cycle G1 phase, which results into a slower proliferation. CLIC1-knockdown can also slow down the tumor growth in vivo. Besides, CLIC1-knockdown cells showed an increased sensitivity to hydrogen peroxide and cisplatin, suggesting that CLIC1 was involved in regulation of redox and drug resistance in ovarian cancer cells. These results indicate CLIC1 promotes tumorgenesis, and is a potential therapeutic target in epithelial ovarian cancer treatment.
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