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:Tumor Microenvironment Modulation by Cancer-Derived Extracellular Vesicles.
Tumor Microenvironment Modulation by Cancer-Derived Extracellular Vesicles.
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肿瘤微环境(TME)在肿瘤发生过程中发挥重要作用,调控癌细胞的生长、代谢、增殖和侵袭,并促进肿瘤对常规放化疗的耐药。在TME中已鉴定出几种表型相对稳定的细胞类型,包括癌相关成纤维细胞(CAFs)、肿瘤相关巨噬细胞(TAMs)、中性粒细胞和自然杀伤(NK)细胞,这些细胞已被证明可调节癌细胞的增殖、转移及与免疫系统的相互作用,从而促进肿瘤异质性。越来越多的证据表明,肿瘤细胞来源的细胞外囊泡(EVs)通过转移各种分子(如RNA、蛋白质、肽和脂质),在TME中正常细胞向肿瘤相关促瘤对应细胞的转化中发挥关键作用。本文综述了EVs在TME调控中的功能,旨在探讨外泌体如何促进正常细胞的转化,以及它们在癌症诊断和治疗中的重要性。
The tumor microenvironment (TME) plays an important role in the process of tumorigenesis, regulating the growth, metabolism, proliferation, and invasion of cancer cells, as well as contributing to tumor resistance to the conventional chemoradiotherapies. Several types of cells with relatively stable phenotypes have been identified within the TME, including cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), neutrophils, and natural killer (NK) cells, which have been shown to modulate cancer cell proliferation, metastasis, and interaction with the immune system, thus promoting tumor heterogeneity.
Growing evidence suggests that tumor-cell-derived extracellular vesicles (EVs), via the transfer of various molecules (e. g. , RNA, proteins, peptides, and lipids), play a pivotal role in the transformation of normal cells in the TME into their tumor-associated protumorigenic counterparts. This review article focuses on the functions of EVs in the modulation of the TME with a view to how exosomes contribute to the transformation of normal cells, as well as their importance for cancer diagnosis and therapy.
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