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Fascin-1 depletion from hepatocellular carcinoma cells inhibits migfilin and vasodilator-stimulated phosphoprotein expression and enhances adhesiona 被引量:1
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作者 Vasiliki Gkretsi Dimitrios P.Bogdanos 《Hepatoma Research》 2016年第1期42-46,共5页
Aim:Extracellular matrix(ECM)-adhesions and their interaction with actin cytoskeleton are fundamental for hepatocellular carcinoma(HCC).Fascin-1,an actin-bundling protein,is correlated with poor HCC prognosis,and is k... Aim:Extracellular matrix(ECM)-adhesions and their interaction with actin cytoskeleton are fundamental for hepatocellular carcinoma(HCC).Fascin-1,an actin-bundling protein,is correlated with poor HCC prognosis,and is known regarding the molecular mechanism of its action.In this study,the authors investigated Fascin-1 basic molecular mechanism and cellular properties in HCC cells.Methods:Fascin-1 was silenced by small interfering RNA and the expression of actin.The ECM-adhesion-related proteins were assessed along with the cells’adhesion capacity in two cell lines that differ in terms of aggressiveness;the hepatoma cell line PLC/PRF/5(Alexander)and the highly invasive HCC cell line HepG2.Results:This study shows that Fascin-1 is upregulated in HepG2 cells compared to Alexander cells and when silenced leads to increased cell adhesion only in HepG2,while at the same time is associated with reduced migfilin and vasodilator-stimulated phosphoprotein(VASP)expression.Conclusion:This is the first study to show that Fascin-1 contributes to a more aggressive phenotype in HCC cells and acts through migfilin and VASP. 展开更多
关键词 ADHESION FASCIN-1 hepatocellular carcinoma migfilin vasodilator-stimulated phosphoprotein
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