CHU Zhi-heng+, HE Shi-yan+, WANG Yu, ZHU Ruo-ting, GU Yi-ling, CHEN Jia-yu

Shaoxing University School of Medicine, Shaoxing 312000, China

Abstract: 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.

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