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目的探讨rapamycin作用于胃癌细胞株MGC-803后对细胞生长影响及其作用机制。方法体外培养胃癌细胞株MGC-803,使用不同浓度rapamycin干预MGC-803细胞。采用MTT法检测细胞增殖变化;实时荧光定量PCR(QPCR)检测关键基因的表达;蛋白印迹法(WB)检测相关蛋白的表达;流式细胞术检测细胞周期及凋亡的变化。结果与对照组相比,rapamycin对胃癌MGC-803细胞的增殖活性有明显的抑制作用,呈现出剂量依赖性(P<0.05)。Rapamycin显著抑制PI3K、AKT、m TOR、4EBP、P70S6K基因的m RNA表达,差异有统计学意义(P<0.05);Rapamycin能抑制p-m TOR、p-P70S6K蛋白的表达;Rapamycin将细胞周期阻滞在G0/G1期,并诱导细胞凋亡(P<0.05)。结论靶向m TOR抑制剂rapamycin可通过调控PI3K/AKT/m TOR信号通路进而调控胃癌细胞的生长。
Objective To investigate the effect of rapamycin on cell growth after gastric cancer cell line MGC-803 and its mechanism. Methods The gastric cancer cell line MGC-803 was cultured in vitro and MGC-803 cells were treated with different concentrations of rapamycin. The cell proliferation was detected by MTT assay. The expression of key genes was detected by real-time fluorescence quantitative PCR (QPCR). The expression of related proteins was detected by Western blotting. The cell cycle and apoptosis were detected by flow cytometry. Results Compared with the control group, rapamycin significantly inhibited the proliferation of gastric cancer MGC-803 cells in a dose-dependent manner (P <0.05). Rapamycin significantly inhibited m RNA expression of PI3K, AKT, mTOR, 4EBP and P70S6K genes (P <0.05), Rapamycin inhibited pm TOR and p-P70S6K protein expression. Rapamycin blocked cell cycle arrest in G0 / G1 phase, and induce apoptosis (P <0.05). Conclusion Targeting the mTOR inhibitor rapamycin can regulate the growth of gastric cancer cells by regulating the PI3K / AKT / m TOR signaling pathway.