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
YTHDF2 在抗肿瘤免疫中的作用
英文原题：The role of YTHDF2 in anti-tumor immunity.
查看英文原题
The role of YTHDF2 in anti-tumor immunity.
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中文摘要
RNA N6-甲基腺苷（m6A）修饰是最丰富的 RNA 修饰，参与多种生理和病理过程。YTHDF2 是首个被发现能够识别 m6A 修饰的阅读蛋白；近期研究还发现，它能够结合 5-甲基胞嘧啶（m5C）修饰。YTHDF2 对 m6A 和 m5C 均具有结合能力，但会导致相反的 mRNA 命运。多项研究强调了 YTHDF2 在肿瘤发生发展及肿瘤微环境中的关键作用。新近证据显示，YTHDF2 参与免疫调节，影响 T 细胞、B 细胞、NK 细胞、巨噬细胞、先天性及适应性抗肿瘤免疫应答，以及基于 T 细胞的免疫治疗。针对 YTHDF2 的抑制剂已经开发，并显示出肿瘤治疗潜力。本文综述 YTHDF2 的分子机制及其在肿瘤、免疫细胞和肿瘤微环境中的作用。
展开英文摘要原文
RNA N 6 -methyladenosine (m 6 A) modification has been identified as the most abundant RNA modification and plays crucial roles in both physiological and pathological processes. YTHDF2 was the first identified reader protein that can recognize m 6 A modification and recent studies also revealed its ability to bind 5-methylcytidine (m 5 C) modification. YTHDF2 shows a dual binding capacity to both m 6 A and m 5 C, which leads to opposite mRNA outcomes.
Multiple studies have highlighted the critical roles of YTHDF2 in tumor development and tumor microenvironment. Emerging findings showed that YTHDF2 plays critical roles in immune regulation, impacting T cell, B cell, NK cell, macrophage, innate/adaptive anti-tumor immune responses, and T-cell based immunotherapy. Inhibitors have been developed to target YTHDF2, which showed potential efficacy in tumor treatment.
Herein, we reviewed the molecular mechanism of YTHDF2 and its roles in tumors, immune cells, and tumor microenvironment.
论文信息
- 作者
- Zhang L、Chen C、Feng J、Zhang H、Nguyen LXT、Chen Z
- 第一作者单位
- Department of Hematological Malignancies Translational Science, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.United States
- 通讯作者单位
- Department of Systems Biology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.United States
- 期刊
- Cell investigation2025 Mar
- 原文标识
- PubMed 40092843 · DOI 10.1016/j.clnves.2025.100008
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