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Propofol inhibits proliferation, migration, and invasion of hepatocellular carcinoma cells by downregulating Twist
Author(s) -
Zheng Haibo,
Fu Yantao,
Yang Tongwei
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28551
Subject(s) - hepatocellular carcinoma , cancer research , twist , propofol , hepatic carcinoma , microbiology and biotechnology , medicine , biology , pharmacology , geometry , mathematics
Abstract Propofol is a commonly used anesthetic drug with potential antitumor activity. The aim of this study was to investigate the antiproliferation and antimetastatic mechanisms of propofol in hepatocellular carcinoma (HCC). SMMC‐7721 was treated with different concentrations of propofol. Cell proliferation was evaluated by the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, and cell motility was assessed by the wound healing assay. Cell migration and invasion ability were analyzed by the transwell assay. Protein levels of E‐cadherin, Vimentin, matrix metalloproteinase 2 (MMP‐2), and MMP‐9 were measured by Western blotting. Twist1 gene expression was assessed by Western blotting and quantitative reverse transcription PCR. The proliferation, motility, migration, and invasion of SMMC‐7721 cells were inhibited by propofol treatment in a dose‐dependent manner. Propofol treatment downregulated the protein levels of Vimentin, MMP‐2, and MMP‐9 while increasing that of E‐cadherin. Propofol treatment inhibited the expression of the Twist1 gene in SMMC‐7721 cells. The overexpression of Twist1 could partially reverse the inhibitory effects of propofol on SMMC‐7721 cells. Propofol inhibited proliferation, migration, and invasion of HCC cells by downregulating the expression of Twist1, making it a potential drug for HCC treatment.