RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Impact of mitochondrial dysfunction on the antitumor effects of immune cells.
Impact of mitochondrial dysfunction on the antitumor effects of immune cells.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
线粒体功能障碍是免疫细胞衰竭的标志,通过代谢重编程、线粒体分裂、融合、生物发生以及免疫检查点信号转导影响免疫细胞的抗肿瘤效应。研究人员认为,恢复受损的线粒体功能可以增强免疫细胞的疗效。然而,癌症患者免疫细胞中线粒体功能障碍的机制尚不清楚。在这篇综述中,我们总结了线粒体功能障碍对T细胞、NK 细胞、树突状细胞和肿瘤相关巨噬细胞抗肿瘤效应的影响,并提出靶向线粒体可以为抗肿瘤治疗提供新策略。
Mitochondrial dysfunction, a hallmark of immune cell failure, affects the antitumor effects of immune cells through metabolic reprogramming, fission, fusion, biogenesis, and immune checkpoint signal transduction of mitochondria. According to researchers, restoring damaged mitochondrial function can enhance the efficacy of immune cells.
Nevertheless, the mechanism of mitochondrial dysfunction in immune cells in patients with cancer is unclear. In this review, we recapitulate the impact of mitochondrial dysfunction on the antitumor effects of T cells, natural killer cells, dendritic cells, and tumor-associated macrophage and propose that targeting mitochondria can provide new strategies for antitumor therapy.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。