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:Decoding the complex web: cellular and molecular interactions in the lung tumour microenvironment.
Decoding the complex web: cellular and molecular interactions in the lung tumour microenvironment.
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。
肺肿瘤微环境(TME)或基质是一个由众多细胞及其释放分子构成的动态空间。这一复杂的网络调控着肿瘤进展以及对不同治疗模式的耐药性。肺癌细胞与其基质共同释放多种因子,削弱先天免疫细胞如自然杀伤(NK)细胞以及效应T细胞适应性应答的抗肿瘤攻击。这些因子包括众多生长因子、外泌体和表观遗传调控因子,以及抗炎细胞因子。理解肿瘤细胞与肺TME内各种元素(如免疫细胞和基质细胞)之间错综复杂的相互作用,有助于提供更好的管理和治疗肺部恶性肿瘤的新策略。本文讨论了介导肺TME通讯的细胞和信号分子的复杂网络。通过阐明这些多方面的相互作用,我们旨在为肺癌治疗的潜在治疗靶点和策略提供见解。
The lung tumour microenvironment (TME) or stroma is a dynamic space of numerous cells and their released molecules. This complicated web regulates tumour progression and resistance to different modalities. Lung cancer cells in conjunction with their stroma liberate a wide range of factors that dampen antitumor attacks by innate immunity cells like natural killer (NK) cells and also adaptive responses by effector T cells. These factors include numerous growth factors, exosomes and epigenetic regulators, and also anti-inflammatory cytokines.
Understanding the intricate interactions between tumour cells and various elements within the lung TME, such as immune and stromal cells can help provide novel strategies for better management and treatment of lung malignancies. The current article discusses the complex network of cells and signalling molecules, which mediate communications in lung TME. By elucidating these multifaceted interactions, we aim to provide insights into potential therapeutic targets and strategies for lung cancer treatment.
MEMBER ACCOUNT
登录成功会直接打开下一页。