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目的 探讨ATRA调节胃癌细胞生长的作用机理。方法 Westernblot测定蛋白表达水平 ,免疫沉淀测定蛋白激酶活性 ,MTT方法检测细胞生长和流式细胞术分析细胞周期。结果 ATRA有效地诱导细胞滞留G0 /G1期并抑制胃癌细胞生长。ATRA通过依赖P5 3和非依赖P5 3途径诱导ATRA敏感细胞的P2 1WAF1/CIP1表达 ,由此导致CDK4 和CDK2 活性下降 ,但对CDK4 和CDK2 蛋白表达没有影响。另外 ,由于ATRA抑制CDK4 和CDK2 活性 ,导致Rb蛋白去磷酸化水平上升。结论 ATRA通过调节细胞周期进程的相关蛋白而抑制胃癌细胞生长。
Objective To explore the mechanism of ATRA regulating the growth of gastric cancer cells. Methods Westernblot was used to determine the protein expression level, immunoprecipitation was used to determine protein kinase activity, MTT assay was used to detect cell growth, and flow cytometry was used to analyze the cell cycle. Results ATRA effectively induced cell retention in G0/G1 phase and inhibited the growth of gastric cancer cells. ATRA induces P2 1WAF1/CIP1 expression in ATRA-sensitive cells through P53-dependent and P53-independent pathways, resulting in decreased CDK4 and CDK2 activity but no effect on CDK4 and CDK2 protein expression. In addition, as ATRA inhibits CDK4 and CDK2 activity, Rb protein dephosphorylation levels increase. Conclusion ATRA inhibits the growth of gastric cancer cells by regulating the relevant proteins of cell cycle progression.