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Chloride intracellular channel 1 (CLIC1) is activated and functions as an oncogene in pancreatic cancer

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Abstract

Chloride intracellular channel 1 (CLIC1), a newly discovered member of the chloride channel protein family, has been implicated in multiple human cancers. However, little is known with regard to its expression and biological functions in pancreatic cancer. In this study, we focused on the clinical significance and biological functions of CLIC1 in pancreatic cancer and found that this protein was overexpressed in pancreatic cancer tissues. Patients with CLIC1-positive tumours had worse overall survival than those with CLIC1-negative tumours. Furthermore, the treatment of pancreatic cancer cell lines with CLIC1-targeting siRNA oligonucleotides significantly reduced cell proliferation and diminished anchorage-independent growth on both soft agar and cell migration. These data indicate that CLIC1 acts as a putative oncogene in pancreatic cancer and may represent a novel diagnostic and therapeutic target for pancreatic cancer.

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Acknowledgments

This work was supported by the National Natural Science Foundation of China (Nos. 81172029, 81272402, and 81402403), the National High Technology Research and Development Program (863 Program) (No. 2012AA022606), the Foundation for Interdisciplinary Research of Shanghai Jiao Tong University (No. YG2011ZD07), the Shanghai Science and Technology Commission Medical-guiding Project (No. 12401905800), the Program for Changjiang Scholars, the Natural Science Foundation of Shanxi Province (Nos. 20110313013-3 and 2014021037-3), and Shanghai Rising-Star Program (No. 15QA1403100).

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The authors have no conflicts of interest to disclose.

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Correspondence to Fei Ma or Jun Gu.

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Jianhua Lu and Qian Dong contributed equally to this work.

Fei Ma and Jun Gu were jointly directed this work.

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Lu, J., Dong, Q., Zhang, B. et al. Chloride intracellular channel 1 (CLIC1) is activated and functions as an oncogene in pancreatic cancer. Med Oncol 32, 171 (2015). https://doi.org/10.1007/s12032-015-0616-9

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  • DOI: https://doi.org/10.1007/s12032-015-0616-9

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