Chloride intracellular channel 1 is an important factor in the lymphatic metastasis of hepatocarcinoma

• Published in: Biomedicine & pharmacotherapy Vol. 66; no. 3; pp. 167 - 172
• Main Authors: Li, Rong-Kuan, Zhang, Jun, Zhang, Yu-Hong, Li, Miao-Ling, Wang, Mei, Tang, Jian-Wu
• Format: Journal Article
• Language: English
• Published: France Elsevier SAS 01.04.2012
• Subjects: Animals; Apoptosis - genetics; Carcinoma, Hepatocellular - genetics; Carcinoma, Hepatocellular - pathology; Cell Division - genetics; Cell Growth Processes - genetics; Cell Line, Tumor; Cell Movement - genetics; Chloride Channels - genetics; CLIC1; Down-Regulation; G2 Phase - genetics; Hepatocarcinoma; Internal Medicine; Liver Neoplasms - genetics; Liver Neoplasms - pathology; Lymphatic Metastasis; Medical Education; Mice; Neoplasm Invasiveness - genetics; RNA interference; RNA, Messenger - genetics; RNA, Small Interfering - genetics; Transfection - methods; Lymphatic metastasis; Hepatocarcinoma; RNA interference; CLIC1
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2011.10.002

Abstract We have previously demonstrated that chloride intracellular channel 1 (CLIC1) is involved in the lymphatic metastasis of tumors. In this study, a self-designed shRNA sequence of mouse CLIC1 gene was synthesized and inserted into a pGPU6/GFP/Neo plasmid, then stably transfected into mouse hepatic carcinoma cell line Hca-F cells to down-regulate the expression of CLIC1 gene. The levels of expression of CLIC1 mRNA and protein were detected by real-time quantitative polymerase chain reaction (qRT-PCR) and western blot (WB) analysis, respectively. The down-regulation of CLIC1 enhanced proliferative activity, increased the ratio of G2/M and decreased percentage of apoptosis. In addition, the capability of migration and invasion decreased significantly. The results indicate that CLIC1 is a critical factor in the development of lymphatic metastasis.