Evodiamine inhibits growth of Huh7 cells and enhances their sensitivity to TRAIL / 中国病理生理杂志

AIM:To investigate the effects of evodiamine on the growth and apoptosis of human hepatocellular carcinoma Huh7 cells,and to illustrate the molecular mechanism that evodiamine enhances antitumor activity of tumors nec -rosis factor-related apoptosis-inducing ligand(TRAIL)in Huh7 cells.METHODS: The cell viability was measured by MTT assay.The cell cycle distribution was analyzed by flow cytometry.The apoptosis rate was determined by TUNEL stai-ning.The protein levels of cell cycle-and apoptosis-related proteins were detected by Western blot analysis.RESULTS:Treatment of Huh7 cells with evodiamine reduced the cell viability(P<0.05).Evodiamine induced cell cycle arrest in G2/M phase by upregulation of p27,cyclin B1, cell division cycle protein 2(Cdc2)and p-Cdc2.Evodiamine triggered apoptosis accompanied by cleavage of caspase-3 and poly(ADP-ribose)polymerase(PARP).Combination of evodiamine with TRAIL significantly reduced the cell viability and increased cleavage of caspase -3 and PARP as compared with the use of each agent alone.Moreover,evodiamine increased the expression of death receptor 5(DR5)in the Huh7 cells.CON-CLUSION:Evodiamine inhibits the cell growth by reducing the cell viability and inducing cell cycle arrest.Evodiamine also triggers cell apoptosis and enhances the sensitivity of Huh 7 cells to TRAIL by upregulating the expression of DR5.

CHK1 inhibitor SCH900776 suppresses proliferation and migration of U251 cells / 中国病理生理杂志

AIM:To investigate the effect of SCH900776, an inhibitor of checkpoint kinase 1(CHK1), on the proliferation and migration abilities of human glioma U 251 cells.METHODS:The cell viability was detected by MTT assay,and cell proliferation was determined by cell colony formation assay.Cell cycle distribution was analyzed by flow cy-tometry.Wound healing assay was used to determine the cell migration ability.The protein levels were determined by Western blot.RESULTS: SCH900776 inhibited the growth of U251 cells in a dose-dependent manner(P <0.05). SCH900776 treatment substantially induced U251 cell cycle arrest in S and G 2/M phases by decreasing the level of cell di-vision cycle protein 2(Cdc2)and p-Cdc2.Moreover,SCH900776 inhibited the cell migration.Western blot results indi-cated that SCH900776 increased the phosphorylation level of p 38 MAPK and inhibited the activation of Akt.CONCLU-SION:SCH900776 inhibits the proliferation and migration abilities in human U 251 cells by promoting the phosphorylation of p38 MAPK and suppressing the activation of Akt.

Inhibition of Caudatin on migration of glioma C6 cells in vitro by downregulating β-catenin/survivin expression / 中草药

Objective: To investigate the effects of Caudatin on cell proliferation and migration of human glioma cell line C6 and the potential mechanisms. Methods: Cell viability was evaluated by MTT assay. Cell cycle distribution was assessed by propidium iodide flow cytometry. Scarification test and Transwell assay were used to measure the cell migration. The effects of Caudatin on the expression of β-catenin, Survivin, CyclinD1, and Cdk4 were determined by Western blotting assay. Results: Caudatin inhibited the C6 cell viability in a dose dependent manner, and caused an accumulation of C6 cells in G1 phase, and Western blotting results suggested that Caudatin inhibited the expression of CyclinD1 and Cdk4. The migration ability of C6 cells was significantly blocked by Caudatin treatment. Caudatin could significantly down-regulate the expression of β-catenin and Survivin in C6 cells. Conclusion: Caudatin could inhibit the C6 cell migration in vitro with a dose dependent way, and the potential mechanism might be related to inhibiting the expression of β-catenin and Survivin in C6 cells.