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首页> 外文期刊>Journal of Cellular Physiology >The STAT3/NFIL3 signaling axis‐mediated chemotherapy resistance is reversed by Raddeanin A via inducing apoptosis in choriocarcinoma cells
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The STAT3/NFIL3 signaling axis‐mediated chemotherapy resistance is reversed by Raddeanin A via inducing apoptosis in choriocarcinoma cells

机译：STAT3 / NFIL3轴信号介导的化疗抵抗由Raddeanin逆转绒毛膜癌的细胞通过诱导细胞凋亡

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摘要

Chemotherapy resistance is the major issue of choriocarcinoma. Apoptosis always is the ultimate outcome of chemotherapeutic drugs, which considered one of the reasons of resistance. We investigated the role of STAT3/NFIL3 signaling‐inhibited apoptosis in chemotherapy resistance and whether Raddeanin A (RA) could be a new drug to reverse resistance. Established three drug‐resistant cell lines as JEG‐3/MTX, JEG‐3/5‐FU, and JEG‐3/VP16. NFIL3 and STAT3 expression was evaluated in the cells. The IC 50 value, apoptosis rate and apoptins were observed with transfection of siNFIL3, Lenti‐OE?‐NFIL3, shSTAT3, and Lenti‐OE?‐STAT3 or RA treatment. In addition, the luciferase reporter analysis and co‐immunoprecipitation assays were used to investigate the relation of STAT3 and NFIL3. Hyper‐activation of STAT3 and NFIL3 expression were observed in three drug‐resistant cell lines. STAT3 enhanced NFIL3 transcriptional activity by binding the relative promoter region. Activated STAT3/NFIL3 pathway caused low rate of apoptosis which resulted in chemotherapy resistance. RA reduced the resistance index of resistant cells and induced caspase 3 dependent apoptosis, meanwhile it repressed the STAT3/NFIL3 activation. STAT3/NFIL3 axis‐inhibited apoptosis is a novel mechanism of chemotherapy resistance in choriocarcinoma. With the suppression of STAT3/NFIL3 axis and apoptosis induction, RA is a potential agent or lead candidate for improving chemotherapy.
机译：化疗抵抗的主要问题绒毛膜癌。化疗药物的结果考虑阻力的原因之一。研究STAT3 / NFIL3的角色信号量抑制细胞凋亡在化疗阻力和是否Raddeanin (RA)一种新药扭转阻力。三个药物耐药细胞系应承担的联合工作组高3 / MTX在JEG‐3 / 5‐是,and JEG‐3 / VP16。表达在细胞评估。值,观察细胞凋亡率和apoptins转染siNFIL3, Lenti OE应承担的吗?shSTAT3, Lenti OE应承担的?的荧光素酶分析和记者公司提供有关免疫沉淀反应化验使用STAT3和NFIL3的关系进行调查。超激活STAT3和NFIL3表达式观察三个药物耐药细胞系。STAT3增强NFIL3转录活动绑定相对启动子区域。STAT3 / NFIL3通路引起的细胞凋亡率较低导致化疗抵抗。耐药细胞的阻力指数降低和诱导半胱天冬酶3相关的细胞凋亡,与此同时它抑制STAT3 / NFIL3激活。是一种新型化疗耐药性的机制绒毛膜癌。STAT3 / NFIL3轴和凋亡诱导,类风湿性关节炎是一个潜在的代理或领先候选人改善化疗。

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