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:Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review).
Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review).
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肿瘤与肿瘤微环境(TME)之间的相互作用在肿瘤发生和肿瘤进展中发挥关键作用。泛素化是调控蛋白质降解和周转的重要翻译后修饰,在调节肿瘤与TME之间的串扰中发挥作用。因此,鉴定泛素化在这一过程中的作用可能有助于研究人员探究肿瘤发生和肿瘤进展的机制。在本综述文章中,总结了关于泛素化底物的新见解,这些底物参与调控缺氧环境、血管生成、慢性炎症介导的肿瘤形成,以及癌症相关成纤维细胞和浸润免疫细胞(肿瘤相关巨噬细胞、T细胞、髓源性抑制细胞、树突状细胞和NK 细胞)的功能。此外,本文还综述并讨论了TME内泛素化蛋白酶体系统用于癌症治疗的潜在靶点及其治疗效果。
The interaction between a tumor and the tumor microenvironment (TME) plays a key role in tumorigenesis and tumor progression. Ubiquitination, a crucial post‑translational modification for regulating protein degradation and turnover, plays a role in regulating the crosstalk between a tumor and the TME.
Thus, identifying the roles of ubiquitination in the process may assist researchers to investigate the mechanisms underlying tumorigenesis and tumor progression.
In the present review article, new insights into the substrates for ubiquitination that are involved in the regulation of hypoxic environments, angiogenesis, chronic inflammation‑mediated tumor formation, and the function of cancer‑associated fibroblasts and infiltrating immune cells (tumor‑associated macrophages, T‑cells, myeloid‑derived suppressor cells, dendritic cells, and natural killer cells) are summarized.
In addition, the potential targets of the ubiquitination proteasome system within the TME for cancer therapy and their therapeutic effects are reviewed and discussed.
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