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基于TRPM4-诱导的过载介导的癌细胞死亡的新型预后模型的开发

Wei Wang¹, Duo Zhao¹, Zijun Zhou¹

¹Second Hospital of Tianjin Medical University, Tianjin, China.

Frontiers in cell and developmental biology

|January 26, 2026

概括

清细胞细胞癌 (ccRCC) 的死亡率很高. 与过载细胞死亡 (NECSO) 相关的TRPM4通道活性显示在ccRCC中具有瘤抑制作用,提供了一个新的预后得分和治疗标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

清细胞细胞癌 (ccRCC) 仍然是一个重大的健康挑战,发病率和死亡率很高.
对于ccRCC,急需新的生物标志物和治疗点.
目前尚不清楚TRPM4通道介导的过载致死 (NECSO) 在ccRCC中的作用.

研究的目的:

调查TRPM4通道在ccRCC中的作用.
开发基于TRPM4相关基因的预后模型.
探索TRPM4,NECSO和ccRCC中的瘤免疫微环境之间的关系.

主要方法:

在KIRC中使用TCGA数据对TRPM4表达的泛癌分析.
基因本体学 (GO) 和KEGG通路丰富分析.
机器学习算法 (plsRcox,GBM,CoxBoost) 用于开发一个14基因的NECSO评分.
使用CIBERSORT,xCell和ESTIMATE进行瘤免疫微环境 (TIME) 评估.
在ccRCC细胞系中TRPM4功能的体外验证.

主要成果:

在KIRC中,TRPM4显著下调,高表达与改善的无复发生存率 (RFS) 相关联.
基于14个基因开发的NECSO评分独立预测了更好的结果,并与激活的免疫微环境联系在一起.
过度表达TRPM4抑制了ccRCC细胞的增殖,迁移和克隆性,同时增强了细胞亡和与Necrocide-1 (NC1) 协同作用,以改善抗瘤作用.

结论:

在ccRCC中,TRPM4表现出瘤抑制作用.
该NECSO评分作为一个强大的预后工具,并突出了平衡和ccRCC免疫力之间的联系.
针对TRPM4和NECSO,为ccRCC提供了一个潜在的治疗策略.

关键词:

TRPM4 TRPM4 在线播放生物信息学是一种生物信息学.细胞死亡是细胞死亡.清细胞细胞癌 (ccRCC) 是一种癌症.预测模型的预测模型.瘤免疫微环境是一个微环境.

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