CtBP1 Is Upregualted In Sarcomatiod Hepatocellular,Associated With Epithelial-tomesenchymal Transition And A Target Of Quercetin Involved In Inhibition Of Migration

Objective: To investigate whether upregulation of CtBP1 is associated with epithelial-to-mesenchymal transition(EMT)in sarcomatiod transformation of hepatocellular carcinoma.To investigate the effection of quercetin on cell migration and expression of CtBP1 and E-cadherin in SMMC-7721 cells.Methods: Immunohistochemistry was used to detect the difference of expression of CtBP1 and EMT associated markers between sarcomatoid areas and classical HCC areas in sarcomatoid hepatocellular carcinoma(sHCC).Wound healing assay was used to detect the migration of cells and western blot used to detect the expression of CtBP1 and E-cadherin in SMMC-7721 cells,which were treated with different concentrations of quercetin(0 、 12.5 、25μmol/L)at different time points.Immunofluorescence was used to detect the expression of CtBP1 and E-cadherin in SMMC-7721 cells after treated with different concentrations of quercetin(0,12.5,25μmol/L).Results: Compared to the classical HCC areas,CtBP1 is upregulated in sHCC areas,and epithelial markers E-cadherin and β-catenin downregulated and mesenchymal marker vimentin upregulated.Quercetin inhibited the migration of SMMC-7721 cells on a dose-and time-dependent manner.Quercetin downregulated the expression of CtBP1 and upregulated the expression of E-cadherin in SMMC-7721 cells by western blot assays.6 hours after quercetin treated,CtBP1 and E-cadherin were immunostained by immnofluorescence,which showed CtBP1 downregulated and E-cadherin upregulated byquercetin in a dose dependent manner.Conclusio-ns: CtBP1 upregulated in sHCC and associated with the EMT-like molecular phenotype,which implying CtBP1 were involved in sarcomatoid transformation of HCC.Quercetin can inhibit migration of SMMCC-7721,which mediated by impaired EMT-like molecular phenotype by downregulating the expression of CtBP1 and upregulating the expression of E-cadherin.