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Effect of Aurora protein kinase inhibitor VX-680 on homogeneity adhe-sion and migration in human hepatoma HepG2 cell / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 945-949,960, 2018.
Article em Zh | WPRIM | ID: wpr-701221
Biblioteca responsável: WPRO
ABSTRACT
AIM:To study the effect of Aurora protein kinase inhibitor VX-680 on homogeneous adhesion and migration ability in human hepatocellular carcinoma cell line HepG 2.METHODS:The HepG2 cell were divided into ex-perimental group and control group, respectively.VX-680 was used in experimental groups at 3 concentrations(3.125 μmol/L group,6.25 μmol/L group and 12.5 μmol/L group).DMSO was used in the control group.The effects of VX-680 at different concentrations on the adhesion ability of human hepatocellular carcinoma HepG 2 cells were observed by cell slow aggregation test and separation experiment.The effects of VX-680 at different concentrations on the migration ability of HepG2 cells was detected by wound healing assay.The expression of E-cadherin in HepG2 cells was detected by Western blot.RESULTS:The results of the slow aggregation test showed that compared with the control group,the number of cell clumps formed in experimental groups was significantly decreased(P<0.01).The results of separation experiment showed that the ratio of NTC/NTEgradually decreased with the increased concentration of VX-680.The results of wound healing as-say showed that as the concentration of VX-680 increased, the cell scratch healing ability gradually weakened compared with control group.The results of Western blot showed that the protein expression of E-cadherin in the HepG2 cells in-creased with the increased concentration of VX-680(P<0.05).CONCLUSION:VX-680 increases the homogeneous ad-hesion and inhibits the migration of HepG 2 cells.
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Pathophysiology Ano de publicação: 2018 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Pathophysiology Ano de publicação: 2018 Tipo de documento: Article