Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 20, Issue 8, Pages 2071-2078Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i8.2071
Keywords
Colon cancer; Intracellular chloride channel 1; Hypoxia-reoxygenation; Reactive oxygen species; Extracellular signal-regulated kinase; Cancer invasion
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Funding
- Eleventh Five-year Plan for Medical Science Development of PLA [06MB243]
- National Natural Science Foundation of China [81101101, 51273165]
- Key Project of Chinese Ministry of Education [212149]
- Projects of Sichuan Province [2010SZ0294, 2011JQ0032, 12ZB038]
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AIM: To investigate the mechanisms of chloride intracellular channel 1 (CLIC1) in the metastasis of colon cancer under hypoxia-reoxygenation (H-R) conditions. METHODS: Fluorescent probes were used to detect reactive oxygen species (ROS) in LOVO cells. Wound healing assay and transwell assay were performed to examine the migration and invasion of LOVO cells. Expression of CLIC1 mRNA and protein, p-ERK, MMP-2 and MMP-9 proteins was analyzed by reverse transcription-polymerase chain reaction and Western blot. METHODS: H-R treatment increased the intracellular ROS level in LOVO cells. The mRNA and protein expression of CLIC1 was elevated under H-R conditions. Functional inhibition of CLIC1 markedly decreased the H-R-enhanced ROS generation, cell migration, invasion and phosphorylation of ERK in treated LOVO cells. Additionally, the expression of MMP-2 and MMP-9 could be regulated by CLIC1-mediated ROS/ERK pathway. CONCLUSION: Our results suggest that CLIC1 protein is involved in the metastasis of colon cancer LOVO cells via regulating the ROS/ERK pathway in the H-R process. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
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