The human lung cancer has high incidence rate and mortality among the carcinoma. The research on enhancing the efficacy of therapy for lung cancer is significant. A resent research found that as a subunit of ESCRT-III...The human lung cancer has high incidence rate and mortality among the carcinoma. The research on enhancing the efficacy of therapy for lung cancer is significant. A resent research found that as a subunit of ESCRT-III, CHMP4C functioned to retard abscission timing to coordinate midbody resolution and prevent accumulation of DNA damage in the abscission checkpoint through phosphorylated by AuroraB. In the current study, we evaluated the possible mechanism of the effects of CHMP4C inhibition on cell cycle and cell survival in A549 cells. We found that CHMP4C knockdown caused lagging S phase in cell cycle through enhancing the phosphorylation of Rb, raising the expression of cyclin B1-cdc2 and suppressing the activation of cyclin A. Meanwhile, CHMP4Cdeletion depressed cell survival via decreasing cell viability and increasing caspase 3/7 activity. This study may promote new significant reference and advance for the mechanism underlying specific function of CHMP4C as well as further research on enhancing therapy effect on non-small lung cancer.展开更多
文摘The human lung cancer has high incidence rate and mortality among the carcinoma. The research on enhancing the efficacy of therapy for lung cancer is significant. A resent research found that as a subunit of ESCRT-III, CHMP4C functioned to retard abscission timing to coordinate midbody resolution and prevent accumulation of DNA damage in the abscission checkpoint through phosphorylated by AuroraB. In the current study, we evaluated the possible mechanism of the effects of CHMP4C inhibition on cell cycle and cell survival in A549 cells. We found that CHMP4C knockdown caused lagging S phase in cell cycle through enhancing the phosphorylation of Rb, raising the expression of cyclin B1-cdc2 and suppressing the activation of cyclin A. Meanwhile, CHMP4Cdeletion depressed cell survival via decreasing cell viability and increasing caspase 3/7 activity. This study may promote new significant reference and advance for the mechanism underlying specific function of CHMP4C as well as further research on enhancing therapy effect on non-small lung cancer.
文摘目的探讨半夏总生物碱(total alkaloids from Pinellia Ternata,TATP)对人肺癌细胞株A549增殖的影响。方法采用四甲基偶氮唑盐(methyl thiazolil tetracolium,MTT)比色法以及集落形成率实验,检测不同浓度的TATP对A549细胞株的生长抑制作用。应用单细胞凝胶电泳分析检测TATP导致A549细胞的DNA损伤情况。结果人肺癌细胞A549经TATP处理后,其体外增殖能力明显下降且与药物的剂量、加药时间呈正相关,与对照组比较,差异均有统计学意义。单细胞凝胶电泳(Single cell gel electrophoresis,SCGE)中,TATP组细胞尾DNA含量、尾长及尾动量与对照组相比差异显著(P<0.01),且呈现浓度依赖性。结论在体外培养的条件下,TATP能明显抑制A549细胞增殖,其机制可能与DNA的损伤作用有关。
