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向瘤内在的SLC16A3,通过瘤免疫微环境重编程来增强抗PD-1的有效性

Ting Yu¹, Zhaoyun Liu², Qingxu Tao³

¹Department of Radiation Oncology and Shandong Provincial Key Laboratory of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, 250117, Shandong, PR China; Department of Oncology, Shandong University Cancer Center, Jinan, 250117, Shandong, PR China; Tianjin Medical University Cancer Institute &Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, PR China; Cancer Center, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, PR China.

|March 24, 2024

概括

向乳酸载体SLC16A3可以克服癌症中的免疫疗法耐药性. 抑制SLC16A3可以降低瘤免疫抑制,并提高抗PD-1疗法的有效性.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
癌症新陈代谢癌症新陈代谢

背景情况:

免疫疗法,特别是免疫检查点抑制剂,已经改变了癌症治疗.
对免疫疗法的耐药性仍然是一个重大的临床挑战.
重编程瘤细胞代谢,特别是糖解,创造了免疫抑制性瘤微环境 (TMEs).

研究的目的:

调查糖溶解在免疫疗法耐药性的作用.
评估SLC16A3 (MCT4) 作为治疗点,以提高免疫疗法的疗效.

主要方法:

对糖溶解相关基因和免疫细胞透的生物信息分析.
评估SLC16A3在癌细胞中的表达及其与抗PD-1反应的相关性.
在临床前模型中SLC16A3的遗传和药理抑制.

主要成果:

高糖分解基因表达与减少CD8+T细胞透和增加骨髓衍生抑制细胞 (MDSCs) 相相关.
在甘油性瘤细胞中,SLC16A3表达升高,与抗PD-1疗效负相关.
抑制SLC16A3降低了乳酸的产生,逆转了TME免疫抑制,并改善了抗PD-1治疗结果.

结论:

由SLC16A3调解的瘤细胞糖解有助于免疫疗法耐药性.
准SLC16A3是一个有希望的策略,可以克服耐药性并增强癌症免疫疗法.

关键词:

葡萄糖溶解是什么? 葡萄糖溶解免疫疗法耐药性免疫疗法耐药性牛奶酸是什么牛奶酸是什么在SLC16A3A3中使用.瘤的免疫微环境

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