吉西他滨对肺癌细胞凋亡及PI3K/AKT信号通路的影响

目的探讨吉西他滨对肺癌细胞凋亡及PI3K/AKT信号通路的影响。方法选取对数生长期的肺癌NCI-H292细胞随机分为吉西他滨组、阿霉素组和对照组,分别采用7μmol/L的吉西他滨、阿霉素与生理盐水处理,采用CCK-8法检测细胞增殖,Transwell小室检测细胞迁移与侵袭,Annexin V-PI双标记法检测细胞凋亡,Western blot实验检测PI3K和AKT蛋白表达。结果细胞处理后24h和48h,吉西他滨组和阿霉素组的细胞增殖指数均低于对照组,吉西他滨组低于阿霉素组,差异均有统计学意义(均P <0.05)。细胞处理后24h和48h,吉西他滨组和阿霉素组的细胞迁移与侵袭指数均低于对照组,吉西他滨组低于阿霉素组,差异均有统计学意义(均P <0.05)。细胞处理后24h和48h,吉西他滨组和阿霉素组的细胞凋亡指数均高于对照组,吉西他滨组高于阿霉素组,差异均有统计学意义(均P <0.05)。细胞处理后24h和48h,吉西他滨组和阿霉素组PI3K和AKT蛋白表达水平均低于对照组,吉西他滨组低于阿霉素组,差异均有统计学意义(均P <0.05)。结论吉西他滨可促进肺癌...

Effects of gemcitabine on apoptosis and PI3K/AKT signaling pathway in lung cancer

Objective To investigate the effects of gemcitabine on apoptosis and PI3K/AKT signaling pathway in lung cancer. Methods NCI-H292 lung cancer cells in the logarithmic growth phase were selected and randomly divided into three groups: a gemcitabine group,a doxorubicin group and a control group,among which 7 μmol/L gemcitabine,doxorubicin and physiological saline,respectively were administered. Cell Counting Kit-8(CCK-8) were used to detect cell proliferation. Transwell chamber was used to detect cell migration and invasion. Annexin V-PI double labeling method was used to detect cell apoptosis.Western blot was used to detect the expression of PI3K and AKT proteins. Results At 24 h and 48 h after cell management,cell proliferation,migration and invasion indexes were lower in gemcitabine group and doxorubicin group than in the control group(all P < 0. 05) and lower in gemcitabine group than in doxorubicin group(all P < 0. 05). Apoptosis indexes were higher in gemcitabine group and doxorubicin group than in the control group and higher in gemcitabine group than in doxorubicin group(all P < 0. 05). The expression of PI3K and Akt protein were lower in gemcitabine group and doxorubicin group than in the control group and lower in gemcitabine group than doxorubicin group(all P < 0. 05). Conclusion Gemcitabine can promote cell apoptosis and inhibit the activation of PI3K/AKT signaling pathway thereby inhibiting cell proliferation,migration and invasion in lung cancer.