Volume 29, Issue 3
DOI: 10.24205/03276716.2020.741
Propofol inhibits Wnt/β-catenin SignalingPathway by Up-regulating mir-219-5b and Its Effect on the Biological Behavior of HepatomaCells
Abstract
Objective: The purpose of this study was to analyze the effect of propofol on the behavior related to the biological of hepatoma cells by up-regulating the signal pathway of Wnt/βCatenin in wingless MMTV integrated website family members (Wnt) by microrna-219-5b (mir219-5b).
Methods: hepatoma cell lines Huh7 and SMMC7721 of human were collected. Some hepatoma cell lines Huh7 of human and SMMC7721 were casually divided into the blank control group (treated with 0μM/ml propofol), the low propofol concentration group (treated with 2μM/ml propofol), the medium propofol concentration group (treated with 5μM/ml propofol), and the high propofol concentration group (treated with 10 μM/ml propofol). The expression level of mir-219-5b protein in each group was compared, and propofol concentration closest to clinical treatment was taken for follow-up experiment. The remaining human hepatoma cell lines, Huh7 and SMMC7721, were randomly divided into three groups: negative control group (transferred into empty corpuscle), propofol group (treated with 5 μ M/ml propofol), mir-219-5b-shrna group (decreased the expression level of mir-219-5b and treated with 5 μM/ml propofol). Cell invasion (cell invasion number), migration ability (number of transmembrane cells), the expression of proteins linked to the Wnt / β-catenin signaling pathway (β-catenin, c-myc) and the proliferation potential (OD value) were compared at day 1, day 2, day 3 and day 4.
Results: In Huh7 and SMMC7721 cells the mean concentration propofol and the high concentration propofol group expression level of mir-219-5b was meaningfully higher than the control group of the blank. So Propofol group concentration is similar to clinical treatment concentration. There was no substantial difference in miR-219-5b expression in Huh7 and SMMC7721 cell lines between the low concentration propofol group and the blank control group. At 2D , 3D and 4D, the 0d values in the propofol group for Huh7 and SMMC7721 cells were meaningfully lower than the negative control group ( P<0.05). At 1D , 2D, 3D and 4D, there was no substantial difference between mir-219-5b-shrna group as well as negative control group in the 0d value of Huh7 and SMMC7721 cells. The number of propofol group Huh7 and SMMC7721 invasion cells and transmembrane cells was significantly lower than those in the negative control group. In propofol therapy, Huh7 and SMMC7721 cells had meaningfully lower levels of protein in β-Catenin and c-myc than the negative control group. In addition, no noteworthy difference in protein levels of Huh7, SMMC7721 β-Catenin, and c-myc between the mir-219-5b-shrna group as well as negative control group. Conclusion: propofol can inhibit Wnt / β-catenin's signaling pathway by up-regulating the expression of mir-219-5b and then hinder the proliferation, along with migration, as well as invasion of hepatoma cells.
Keywords
Propofol, mir-219-5b, Wnt, β-Catenin.