Gelsolin (GSN), one of the most important actin structure regulating proteins, has been implicated in the oncogenesis of some cancers. In this study, we investigated the expression of GSN in hepatocellular carcinoma (HCC) and revealed its potential mechanisms. The mRNA and protein levels of GSN were overexpressed in HCC cells and HCC tissues compared to adjacent noncancerous tissues. GSN expression was correlated with venous invasion (P=0.0199) and Edmonson grading (P=0.0344) expression in HCC. Overexpression of GSN in Huh7 and SMMC-7721 cells significantly promoted cell proliferation and the number of Matrigel™-invading cells compared with control cells, with increased expression of matrix metalloproteinase MCL-1, MMP-2 and MMP-9, a key regulator of growth and invasion. In contrast, knockdown of GSN expression with small interfering RNA (siRNA) in MHCC-97L and MHCC-97H cell lines resulted in decreased cell viability and cell invasion. Our findings indicated that GSN expression promoted tumor-associated phenotypes by facilitating proliferative and invasive capacities of HCC cells, which might serve as a potential therapeutic target for HCC treatment.
Keywords: Cell invasion; Cell proliferation; GSN; HCC.
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