[Effects of Astragalin on apoptosis of undifferentiated gastric cancer cells].

OBJECTIVE: To investigate the effects and related molecular mechanisms of Astragalin on undifferentiated gastric cancer cell HGC-27. METHODS: Astragalin was used to treat HGC-27 cells, the cell proliferation activity was detected by CCK-8 method, the cell morphology was observed under inverted microscope, hoechst 33342 and JC-1 staining were used to observe the changes of nucleus formation and mitochondrial membrane potential, the cell cycle and apoptosis rate were detected by flow cytometry, the reverse transcription level of the gene was analyzed by the second-generation sequencer. RESULTS: Astragalin inhibited the proliferation of HGC-27 significantly (P＜0.01), down-regulated mitochondrial membrane potential, induced cell apoptosis, blocked the cell cycle in G1 prophase. At the same time, Astragalin up-regulated the transcription levels of genes bax and bad, down-regulated the transcription levels of genes egf, egfr, pik3cb, pdk1, akt3 and bcl-2. Western blot analysis also showed that the expressions of PI3K and Akt protein were decreased, and the proportion of Bax and BCL-2 protein was increased significantly (P＜0.01). CONCLUSION: The apoptosis of undifferentiated gastric cancer cell line HGC-27 can be induced by Astragalin through inhibition of EGFR/PDK/Akt signaling pathway, and the cell cycle can be blocked in G1 phase, which has a certain therapeutic effect on undifferentiated gastric cancer.

[The effects of shikonin on liver cancer cells SMMC-7721 apoptosis and its mechanism].

Objective: To investigate the effects and molecular mechanisms of shikonin on liver cancer SMMC-772 cells. Methods: SMMC-7721 cells were treated with shikonin at the concentrations of 0, 5, 20, 80 and 320 ng/ml for 0, 24, 48 and 72 h respectively. The proliferative activity of the cells was detected by CCK8 assay. The nuclear type changes of cells was observed after hoechst 33342 staining. Flow cytometry was used to analyze cell apoptosis and death rate. The expressions of proteins in cells were determined by Western blot, and the tumor inhibitive effects were observed through anti-tumor experiment on the BALB/c mice. Results: In vitro experiments, shikonin could inhibit the proliferation of SMMC-7721 cells and induce their apoptosis(P＜0.01), up-regulate the expression of p53 gene, down-regulate the phosphorylation levels of AKT and PI3K protein. In vivo study also confirmed that shikonin could significantly inhibit the growth of tumor in tumor-bearing mice(P＜0.01)in dose-dependent and time-dependent manners. Conclusion: Shikonin can inhibit the proliferation activitity and induce apoptosis of SMMC-7721 cells by affecting the PI3K/AKT signal pathway and has potential anti-liver cancer functions.