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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-2and 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.
AIM: To investigate the mechanisms of chloride intracellular channel 1 (CLIC1) in the metastasis of colon cancer under hypoxia-reoxygenation (HR) conditions. METHODS: Fluorescent probes were used to detect reactive oxygen species (ROS) in LOVO cells. 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 were analyzed by reverse transcription- polymerase chain reaction and Western blot. METHODS: HR treatment increased the intracellular ROS level in LOVO cells. The mRNA and protein expression of CLIC1 was elevated under HR conditions. Functional inhibition of CLIC1 markedly decreased the HR-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 LOV O cells via regulating the ROS / ERK pathway in the H-R process.