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Original Article




           Fascin-1 depletion from hepatocellular carcinoma cells inhibits


           migfilin and vasodilator-stimulated phosphoprotein expression
           and enhances adhesiona



                            1
           Vasiliki Gkretsi , Dimitrios P. Bogdanos    1,2,3
           1 Department of Biomedical Research and Technology, Institute for Research and Technology-Thessaly, Centre for Research and
           Technology-Hellas (CE.R.T.H.), 41222 Larissa, Greece
           2 Department of Rheumatology, School of Medicine, University Hospital of Larissa, University of Thessaly, 41110 Larissa, Greece
           3 Department of Liver Studies and Transplantation, Institute of Liver Studies, King’s College Hospital, Denmark Hill, London SE5
           9RS, UK



                ABSTRACT
                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.
                Key words: Adhesion; Fascin-1; hepatocellular carcinoma; migfilin; vasodilator-stimulated phosphoprotein

           Address for correspondence:
           Dr. Vasiliki Gkretsi, Department of Biomedical Research and Technology, Institute for Research and Technology-Thessaly, Centre for Research
           and Technology-Hellas (CE.R.T.H.), 51 Papanastasiou Street, 41222 Larissa, Greece. E-mail: vasso.gkretsi@gmail.com
           Received: 23-05-2015, Accepted: 09-10-2015




                                Dr. Vasiliki Gkretsi received her BSc in Biology from the University of Athens, Greece (2001) and
                                her Ph.D from the University of Pittsburgh Medical School, USA (2006). She has received numerous
                                awards and published 21 papers (h index = 12). Her research focuses on the role of extracellular
                                matrix, and cell adhesion in metastasis.






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                                                               How to cite this article: Gkretsi V, Bogdanos DP. Fascin-1 depletion
                                                               from  hepatocellular  carcinoma  cells  inhibits  migfi  lin  and  vasodilator-
            DOI:                                               stimulated phosphoprotein expression and enhances adhesion.
            10.4103/2394-5079.168071                           Hepatoma Res 2016;2:42-6.


            42                                                 © 2016 Hepatoma Research | Published by OAE Publishing Inc.
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