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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.

Fascin-1 depletion from hepatocellular carcinoma cells inhibits migfilin and vasodilator-stimulated phosphoprotein expression and enhances adhesion