...
首页> 外文期刊>Cancer letters >Targeting ER stress induced apoptosis and inflammation in cancer
【24h】

Targeting ER stress induced apoptosis and inflammation in cancer

机译:靶向内质网应激诱导癌症的凋亡和炎症

获取原文
获取原文并翻译 | 示例
           

摘要

Disturbance in the folding capacity of the endoplasmic reticulum (ER), caused by a variety of endogenous and exogenous insults, prompts a cellular stress condition known as ER stress. ER stress is initially shaped to re-establish ER homeostasis through the activation of an integrated intracellular signal transduction pathway termed as unfolded protein response (UPR). However, when ER stress is too severe or prolonged, the pro-survival function of the UPR turns into a toxic signal, which is predominantly executed by mitochondrial apoptosis. Moreover, accumulating evidence implicates ER stress pathways in the activation of various 'classical' inflammatory processes in and around the tumour microenvironment. In fact, ER stress pathways evoked by certain conventional or experimental anticancer modalities have been found to promote anti-tumour immunity by enhancing immunogenicity of dying cancer cells. Thus, the ER functions as an essential sensing organelle capable of coordinating stress pathways crucially involved in maintaining the cross-talk between the cancer cell's intracellular and extracellular environment. In this review we discuss the emerging link between ER stress, cell fate decisions and immunomodulation and the potential therapeutic benefit of targeting this multifaceted signaling pathway in anticancer therapy.
机译:由各种内源性和外源性损伤引起的内质网(ER)折叠能力的紊乱会引发称为ER应激的细胞应激状态。 ER应激最初通过激活整合的细胞内信号转导途径(称为未折叠的蛋白应答(UPR))来重建ER稳态。但是,当ER压力过大或过长时,UPR的促生存功能会转变为毒性信号,主要由线粒体凋亡执行。此外,越来越多的证据表明,ER应激途径参与了肿瘤微环境中及其周围各种“经典”炎症过程的激活。实际上,已经发现由某些常规或实验性抗癌方式引起的ER应激途径通过增强垂死的癌细胞的免疫原性来促进抗肿瘤免疫。因此,ER发挥了重要的传感细胞器的作用,能够协调应力通路,这些应力通路与维持癌细胞的细胞内和细胞外环境之间的相互影响至关重要。在这篇综述中,我们讨论了内质网应激,细胞命运决定和免疫调节之间的新兴联系,以及在抗癌治疗中靶向这种多方面信号通路的潜在治疗益处。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号