RNA splicing meets anti-tumor immunity

Miguel Foronda

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RNA splicing meets anti-tumor immunity

机译：RNA剪接满足抗肿瘤免疫力

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Spliceosome-targeted therapies (STTs) drive cancer cell death by promoting widespread alterations to RNA splicing. Although some mis-spliced candidates have been linked to therapeutic responses to STTs, generalized mechanisms of tumor cell cytotoxicity after global defective splicing remain unclear. Νhis year, two independent studies by Νowling et al. and by Lu et al. provided key mechanistic insights into the adaptive anti-tumor immune responses elicited by pharmacological inhibition of spliceosomes, by connecting the responses to increased neoantigen presentation and the induction of pathways that sense double-stranded RNA (dsRNA) in tumor cells.

机译：Spliceosome-targeted治疗癌症(stt)驱动器细胞死亡通过促进广泛的变化RNA剪接。候选人与治疗反应stt,广义的机制全球有缺陷的肿瘤细胞后的细胞毒性拼接仍不明朗。独立研究Ν违禁品的走私等人陆等人提供的关键机械的见解自适应抗肿瘤免疫反应引起剪接体的药物抑制连接反应neoantigen增加表示和通路的感应双链RNA(极)的肿瘤细胞。

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《Nature cancer.》 |2021年第12期|1287-1287|共1页
作者
Miguel Foronda;
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Neoplastic Cell; Spliceosomes; tumor immunitydouble stranded RNAImmunityneoantigensresponse to treatmentCell Deathaluminium;

机译：肿瘤细胞;剪接体;肿瘤immunitydouble困RNAImmunityneoantigensresponse来treatmentCell Deathaluminium;

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专利

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RNA splicing meets anti-tumor immunity

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