摘要
目的:研究PERK-ATF4通路的激活水平,以探讨布雷菲德菌素A(BFA)与顺铂(CDDP)的协同抗肺癌的分子机制。方法:以BFA、CDDP单独或联合处理人肺癌GLC-82细胞24、48 h,然后用定量PCR和Western Blot检测PERK、ATF4、p-PERK的表达水平。结果 :药物处理24和48 h后,GLC-82细胞PERK的m RNA和蛋白表达水平在CDDP组最低,在BFA组升高(P<0.05),在BFA+CDDP组进一步升高(P<0.01),其磷酸化水平均显著降低(P<0.01);ATF4表达在CDDP组中差异无显著性,在BFA组中升高,在BFA+CDDP组进一步升高(P<0.05或P<0.01),也高于BFA组和CDDP组(P<0.05或P<0.01)。结论 :BFA联合CDDP上调PERK、ATF4水平,该通路可能是BFA与顺铂协同抗肺癌的分子机制之一。
Objective To investigate the molecular mechanisms of synergistic effects of BFA and CDDP on human lung cancer GLC-82 cells, and to test the levels of PERK-ATF4 pathway. Methods GLC-82 cells were incubated with 50 ng / m L of BFA or / and 2 μg / m L of CDDP for 24 or 48 hours. The levels of PERK, p-PERK and ATF4 in GLC-82 were analyzed by real-time PCRand / or Western Blot. Results The levels of PERK were lowest in CDDP group, but higher in BFA group（P〈 0.05）, the highest in group of BFA＋CDDP（P〈 0.05 or P〈 0.01）. The p-PERK level decreased in group of BFA ＋CDDP（P〈 0.05 or P〈 0.01）. There was no significant change of ATF4 expression in CDDP group, but ATF4 expression increased slightly in BFA group,and increased further in group of BFA ＋CDDP（P〈 0.05 or P〈 0.01）which was also higher than that in BFA group or CDDP group（P〈 0.05 or P〈 0.01）. Conclusions The upregulated levels of PERK and ATF4 by the combination of BFA and CDDP may be one of the mechanisms of synergistic anti-cancer effect of BFA and CDDP on GLC-82 cells.
出处
《实用医学杂志》
CAS
北大核心
2016年第14期2302-2305,共4页
The Journal of Practical Medicine
基金
贵州省科技厅资助项目(编号:黔科合J字[2013]2319号
黔科合LH字[2014]7548号)
贵州省教育厅特色药用资源研发创新团队(编号:黔科合人才团队字[2013]15)
遵义医学院博士启动基金(编号:F-655)
遵义医学院遗传学扶持学科经费(编号:2012-2016)
