Résumé
ObjectiveTo study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer (CRC) cells by regulating the phosphatase and tensin homolog deleted on chromosome ten (PTEN)/phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (Akt) signaling pathway. MethodShenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured in vitro, and treated with different concentrations of Shenbai Jiedu prescription (2, 4, 8, 16 g·L-1). The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium (MTT). Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN, PI3K, Akt, glycogen synthase kinase-3β (GSK-3β), c-Myc, survivin and Cyclin D1. Western blot was employed to measure the protein expression levels of PTEN, phosphorylated PTEN (p-PTEN), PI3K, Akt, phosphorylated Akt (p-Akt), GSK-3β, phosphorylated GSK-3β (p-GSK-3β), c-Myc, survivin and Cyclin D1, β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group, Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner (P<0.01). Compared with the control group, the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K, Akt, c-Myc, survivin and CyclinD1 were down-regulated after treatment with Shenbai Jiedu prescription (P<0.01). The protein expression levels of PTEN, p-PTEN and GSK-3β were up-regulated whereas those of PI3K, Akt, p-Akt, GSK-3β, p-GSK-3β, c-Myc, survivin and CyclinD1 were down-regulated (P<0.05, P<0.01). Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.