Abstract

To clarify the effect of Nischarin on the biological behavior of hepatocellular carcinoma cells, two human hepatocellular carcinoma cell lines QGY-7701 and HepG2 were selected. The migration ability of the cells was determined with human normal hepatocyte LO2 as control. Western blotting was used to detect the differential expression of Nischarin and its downstream signals. The expression of Nischarin was knocked down by plasmid transfection to study the changes of cell migration ability, so as to evaluate the effect of Nischarin on hepatocellular carcinoma cells. The results of cell scratch experiment showed that compared with LO2 cells, the migration ability of HepG2 was significantly enhanced (<I>P </I>< 0.05), but there was no significant difference in the migration ability between QGY-7701 and LO2 cells. The results of Western blotting showed that the expression of Nischarin in HepG2 was significantly lower than that in LO2 cells (<I>P</I> < 0.05). Quantitative RT-PCR was used to detect the mRNA level of Nischarin in cells and found that the Nischarin mRNA level of HepG2 was significantly lower than that of LO2 (<I>P</I> < 0.01). When HepG2 cells were transfected with Nis-shRNA to knock down the expression of Nischarin, the cell migration ability was significantly increased (<I>P</I> < 0.05). While Nischarin overexpression significantly inhibited the phosphorylation of LIMK1 and cofilin, the important molecules of Rho-GTPase signaling pathway. These results strongly suggest that Nischarin is an endogenous protein with the ability to inhibit the migration of hepatocellular carcinoma cells. In conclusion, we found a protein that can inhibit the migration of hepatocellular carcinoma cells, which may have potential value in the diagnosis and treatment of hepatocellular carcinoma, but its molecular mechanism needs to be further studied.

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