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Effect and mechanism of total flavones of oldenlendia diffusa willd on epithelial-mesenchymal transition of cell line MHCC97-H induced by TGF-β1 / 西安交通大学学报(医学版)
Article em Zh | WPRIM | ID: wpr-603610
Biblioteca responsável: WPRO
ABSTRACT
ABSTRACT:Objective To investigate the effects of total flavones of oldenlandia diffusa (FOD)on epithelial-mesenchymal transition in hepatocellular cancer cell line MHCC97-H.Methods TGF-β1 induced EMT in routinely cultured liver cancer cell line MHCC97-H;then MHCC97-H cell was divided into 5 groups:normal control group, TGF-β1 group,TGF-β1 + FOD group,TGF-β1 + 5-FU group,and TGF-β1 + FOD + 5-FU group.After 48 h of treatment,the invasion ability of MHCC97-H cell was detected by Transwell;the proteins of E-cadherin and vimentin were determined by Western blot.Results Compared with the normal form of MHCC97-H cell line,the cell had obvious long fusiform after TGF-β1 induction,and the invasion ability enhanced (P = 0.02 ).But after treatment,the invasion ability of MHCC97-H cell decreased in FOD group and 5-FU group compared with that in TGF-β1 group (P = 0.03,P = 0.02 ),and decreased more significantly in FOD + 5-FU group (P = 0.01 ).The expression of E-cadherin at the protein level decreased significantly (P = 0.01 )in TGF-β1 group,which was abolished in FOD group (P =0.03 )and 5-FU group (P = 0.02 ).The expression of vimentin at the protein level increased significantly (P =0.01)in TGF-β1 group,which was abolished in FOD group (P =0.04)and 5-FU group (P =0.03)and more obviously in FOD+5-FU group (P =0.01).Conclusion FOD can reverse the invasion of MHCC97-H cells in EMT induced by TGF-β1 through decreasing the expression of E-cadherin protein and inhibiting the epithelial-mesenchymal transition of MHCC97-H cell.
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Journal of Xi'an Jiaotong University(Medical Sciences) Ano de publicação: 2016 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Journal of Xi'an Jiaotong University(Medical Sciences) Ano de publicação: 2016 Tipo de documento: Article