Effect Of Recipe Of Antiliver Cancer On PI3K/AKT Pathway Of Human Hepatoma Cells SMMC-7721

ObjectiveThe purpose of our study was to investigate mechanism of action of ALC in the human Hepatoma Cells SMMC-7721,and then to explain the molecular basis on the theory of "cancer toxin" from professor Zhou Zhongying.The result established the basis the clinical research and clinical application in the future.MethodsThe anti-proliferative potential of ALC was assessed using MTT assay. The expressions of cell cycle proteins and apoptosis-associated proteins were detected by flow-cytometric analysis.Cell apoptosis and the apoptosis-related protein activation of PI3K/AKT pathway in human Hepatoma Cells SMMC-7721were evaluated by RT-PCR and Western Blot after treatment with ALC.ResultsALC suppressed the proliferation of human Hepatoma Cells SMMC-7721in a time and dose-dependent manner. Apoptotic cells could be found under the microscope. The analysis of cell cycle indicated that ALC and its decomposed recipes blocked cells at G0/G1phases and the cells of S and G2/M Phase reduced which confirmed the induction of apoptosis by ALC.RT-PCR and Western Blot showed that the activation of caspase-9,upregulation of PTEN and downregulation of AKT in ALC-treated human Hepatoma Cells SMMC-7721.ConclusionALC could inhibit the proliferation of the hepatoma cell line SMMC-7721.Cells were blocked at G0/G1phases.ALC may suppress constitutively activated targets of phosphatidylinosito-1-3-kinases(PI3K) and AKT, whereafter activate caspase-9in the human Hepatoma Cells SMMC-7721through increasing the activation of PTEN, which suggested that PI3K/Akt pathway plays an important roles in ALC-induced apoptosis of human Hepatoma Cells SMMC-7721.