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:Mechanisms of TREM2 mediated immunosuppression and regulation of cancer progression.
Mechanisms of TREM2 mediated immunosuppression and regulation of cancer progression.
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癌症免疫治疗近期已成为癌症治疗的重要策略。TREM2 是调节肿瘤免疫微环境的关键靶点,对癌症治疗和进展均具有重要作用。TREM2 是免疫信号枢纽,可调节多条病理通路:它不仅可抑制 T 细胞介导的免疫应答,削弱抗肿瘤免疫,还可通过影响 NK 细胞介导的抗肿瘤免疫影响肿瘤发生。值得注意的是,不同肿瘤细胞中的 TREM2 表达水平差异显著,并可通过调节多种信号通路控制肿瘤进展。本文总结 TREM2 在癌症免疫治疗中的作用及其调控肿瘤进展的机制,阐明 TREM2 在肿瘤进展和癌症治疗中的意义,并确定其作为肿瘤疾病新治疗靶点的潜力。
Cancer immunotherapy has recently emerged as a key strategy for cancer treatment. TREM2, a key target for regulating the tumor immune microenvironment, is important in cancer treatment and progression. TREM2 is an immune signaling hub that regulates multiple pathological pathways. It not only suppresses anti-tumor immune responses by inhibiting T cell-mediated immune responses, but it also influences tumorigenesis by affecting NK cell-mediated anti-tumor immunity.
Noticeably, TREM2 expression levels also vary significantly among different tumor cells, and it can regulate tumor progression by modulating various signaling pathways. Above all, by summarizing the role of TREM2 in cancer immunotherapy and the mechanism by which TREM2 regulates tumor progression, this paper clarifies TREM2's role in both tumor progression and cancer therapy, identifying a new therapeutic target for oncology diseases.
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