Overexpression of HBXIP in HepG2 cells induces cell migration and regulates expression of β-catenin |
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Authors: | CUI Li-yuan ZHANG Zhao-rui FEI Hong-rong YAO Shu-tong LI Xiao-qian WANG Feng-ze |
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Affiliation: | 1. School of Biological Sciences, Taishan Medical University, Taian 271016, China;2. School of Pharmacy, Taishan Medical University, Taian 271016, China;3. School of Basic Medical Sciences, Taishan Medical University, Taian 271016, China |
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Abstract: | AIM: To investigate the effects of hepatitis B virus X-interacting protein(HBXIP) in hepatic cancer cells on the cell migration and expression of β-catenin. METHODS: Transwell assay was used to assess the cell migration. Gelatin zymography was used to observe the activity of matrix metalloproteinase 9 (MMP-9). The expression of MMP-9, glycogen synthase kinase 3β(GSK-3β), p-GSK3β, β-catenin and p-β-catenin in HepG2 cells was determined by Western blotting. RESULTS: HepG2 cells which stably overexpressed HBXIP (HepG2-HBXIP) exhibited higher migration ability than the control cells. The results of the gelatin zymography assay showed that HBXIP overexpression increased the activity of MMP-9 in HepG2 cells. The results of Western blotting indicated that HBXIP increased the expression of MMP-9 and β-catenin, inhibited the phosphorylation of β-catenin and promoted the phosphorylation of GSK-3β (Ser9). CONCLUSION: HBXIP regulates the GSK-3β/β-catenin signaling pathway, resulting in a significant improvement of hepatocellular carcinoma cell migration. |
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Keywords: | Liver neoplasms Hepatitis B virus X-interacting protein Matrix metalloproteinase 9 β-catenin |
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