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
TRAIL 信号在癌症和免疫中的多方面作用
英文原题：The multifaceted role of TRAIL signaling in cancer and immunity.
查看英文原题
The multifaceted role of TRAIL signaling in cancer and immunity.
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中文摘要
肿瘤坏死因子（TNF）相关凋亡诱导配体（TRAIL）是TNF超家族成员，可诱导肿瘤细胞或感染细胞凋亡。然而，激活TRAIL信号也可能在癌细胞和未转化细胞（即免疫细胞）中触发非凋亡通路。本文综述当前对非经典TRAIL信号的认识，介绍并解释TRAIL信号在免疫细胞和恶性细胞中的生物学结局，并重点讨论TRAIL对自然杀伤（NK）细胞功能的作用。此外，文章强调了解析凋亡与非凋亡TRAIL信号切换中精确分子机制的技术困难。最后，作者讨论治疗性调节癌症中TRAIL的后果，并提出可能绕开这些困难的方法。
展开英文摘要原文
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that can lead to the induction of apoptosis in tumor or infected cells.
However, activation of TRAIL signaling may also trigger nonapoptotic pathways in cancer and in nontransformed cells, that is, immune cells.
Here, we review the current knowledge on noncanonical TRAIL signaling. The biological outcomes of TRAIL signaling in immune and malignant cells are presented and explained, with a focus on the role of TRAIL for natural killer (NK) cell function.
Furthermore, we highlight the technical difficulties in dissecting the precise molecular mechanisms involved in the switch between apoptotic and nonapoptotic TRAIL signaling.
Finally, we discuss the consequences thereof for a therapeutic manipulation of TRAIL in cancer and possible approaches to bypass these difficulties.
论文信息
- 作者
- Cardoso Alves L、Corazza N、Micheau O、Krebs P
- 单位
- Institute of Pathology, University of Bern, Switzerland.Switzerland
- 文献类型
- 非美国政府资助研究 · 综述
- 期刊
- The FEBS journal2021 Oct
- 原文标识
- PubMed 33215853 · DOI 10.1111/febs.15637