Abstract
Hepatocellular carcinoma is a cancer with high incidence and mortality, and metastasis is a major factor leading to cancer-related mortality. Hepatocellular carcinoma cells are morphologically different from normal liver cells. Plectin can affect cellular architecture by modulation of cytoskeletal organization. Plectin also participates in regulating mitogen-activated protein kinase cascades and the PKC signaling pathway leading to cell migration. In epithelial cells, cytokeratins are connected by plectin to the hemidesmosomes serves as an anchorage between cell and matrix. Our previous studies demonstrated that plectin-deficiency-mediated pleomorphism is associated with an altered level of cytokeratin18 expression in hepatocellular carcinoma. Therefore, we proposed a hypothesis that whether plectin deficiency in hepatocellular carcinoma modulate cell motility and tumor metastasis. In this study, the significance of plectin deficiency among liver and hepatoma cell lines will be analyzed for cell migration. The results of Western blot analyses and immunofluorescent assay demonstrated that the expression of plectin was higher in Chang liver cells but lower in PLC/PRF/5 hepatoma cells and were lowest in HepG2 hepatoma cells. Trans-well migration assay revealed that HepG2 cells had the higher rate of cell migration and followed by PLC/PRF/5 cells, while Chang liver cells had the lowest migration rate. Furthermore, the expression of E-cadherin was higher in HepG2 cells but lower in PLC/PRF/5 cells and was lowest in Chang liver cells. The results of collecting migration assay were also correlated with the expression pattern of E-cadherin among these cell lines. In conclusion, we suggested that plectin deficiency and E-cadherin overexpression in hepatoma cells was related to the higher cell motility and higher collecting migration of these cells. Plectin might affect the regulation of cell motility involved in the invasiveness of hepatocellular carcinoma.
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