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向SRSF1可以通过对CD8⁺T和瘤细胞的双重作用来改善癌症免疫疗法

Gui-Qi Zhu^1,2, Zheng Tang^1,2, Tian-Hao Chu^1,2

¹Department of Liver Surgery and Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University; Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, China.

Signal transduction and targeted therapy

|January 21, 2025

概括

在癌细胞中准拼接因子SRSF1可以增强CD8+T细胞免疫力和新陈代谢. 抑制SRSF1可以提高抗瘤反应和免疫疗法的有效性,从而提供一种新的治疗策略.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

氨酸氨酸丰富拼接因子1 (SRSF1) 是一种致癌拼接因子,驱动癌症进展.
抑制瘤内在SRSF1对抗瘤免疫力的影响尚不清楚.

研究的目的:

研究SRSF1抑制对瘤微环境和CD8+T细胞介导免疫的作用.
探索SRSF1作为增强癌症免疫疗法的治疗标.

主要方法:

在CD8+ T细胞和瘤细胞中减少SRSF1.
对基因转录因子 (c-Jun,c-myc,JunB) 和糖溶性代谢的分析.
在小鼠癌症模型中使用SRSF1小分子抑制剂TN2008的治疗.
评估CD8+T细胞功能和采用T细胞治疗的疗效.

主要成果:

降低CD8+T细胞中的SRSF1的含量,改善了它们的免疫功能和糖溶性新陈代谢.
在瘤细胞中禁用SRSF1减少了关键的转录因子,重编程了新陈代谢并恢复了CD8+ T细胞的功能.
TN2008治疗增强了抗瘤免疫反应,并在体内增强了免疫治疗的有效性.

结论:

准SRSF1同时破坏瘤细胞代谢,并增强CD8+ T细胞抗瘤免疫力.
抑制SRSF1是一种有前途的策略,可以改善癌症免疫治疗的结果.

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