Affiliation:
1. Department of Oncology, The Affiliated Wujin Hospital Jiangsu University Changzhou Jiangsu People's Republic of China
2. School of Life Sciences Jiangsu University Zhenjiang Jiangsu People's Republic of China
3. Department of Oncology Wujin Clinical College of Xuzhou Medical University Changzhou Jiangsu People's Republic of China
Abstract
AbstractAs a master transcription factor, c‐Myc plays an important role in promoting tumor immune escape. In addition, PPARγ (peroxisome proliferator‐activated receptor γ) regulates cell metabolism, inflammation, and tumor progression, while the effect of PPARγ on c‐Myc‐mediated tumor immune escape is still unclear. Here we found that cells treated with PPARγ agonist pioglitazone (PIOG) reduced c‐Myc protein expression in a PPARγ‐dependent manner. qPCR analysis showed that PIOG had no significant effect on c‐Myc gene levels. Further analysis showed that PIOG decreased c‐Myc protein half‐life. Moreover, PIOG increased the binding of c‐Myc to PPARγ, and induced c‐Myc ubiquitination and degradation. Importantly, c‐Myc increased PD‐L1 and CD47 immune checkpoint protein expression and promoted tumor immune escape, while PIOG inhibited this event. These findings suggest that PPARγ agonist inhibited c‐Myc‐mediated tumor immune escape by inducing its ubiquitination and degradation.
Funder
National Natural Science Foundation of China
Subject
Cell Biology,Molecular Biology,Biochemistry
Cited by
5 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献