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TRPM7通过STAT3对FOSL1基因进行交换激活,并增强质瘤干性

Shanchun Guo¹, Vanajothi Ramar², Alyssa A Guo³

¹Department of Chemistry, Xavier University, 1 Drexel Dr, New Orleans, LA, USA.

Cellular and molecular life sciences : CMLS

|August 29, 2023

概括

TRPM7通过通过STAT3.3激活FOSL1转录来调节质瘤茎度. 与ALDH1和TRPM7一起,FOSL1是质瘤的潜在诊断标记物和治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

TRPM7 (过时受体潜力美拉斯7) 通过STAT3信号参与调节质瘤干.
FOSL1被确定为TRPM7的反应基因,并作为促进质瘤扩散和入侵的瘤基因.

研究的目的:

阐明TRPM7通过FOSL1.1影响质瘤干的机制.
研究FOSL1在维持质瘤干细胞 (GSC) 特性中的作用.
评估TRPM7,ALDH1和FOSL1在质瘤患者中的临床相关性.

主要方法:

流细胞计和极限限稀释试验 (ELDA) 来评估GSC标记物和干细胞活性.
路西法酶记者测定和ChIP-qPCR分析FOSL1促进剂活性和STAT3结合.
在质瘤患者的组织微阵列 (TMA) 上进行免疫组织化学 (IHC) 染色.

主要成果:

FOSL1敲击降低了GSC标记物 (CD133,ALDH1) 和干细胞活性.
在FOSL1促进体中,STAT3与特定GAS元素的结合对于其通过TRPM7.7激活至关重要.
在患者中,TRPM7,ALDH1和FOSL1蛋白表达与质瘤等级以及彼此相关.

结论:

由STAT3介导的TRPM7诱导的FOSL1转录激活是质瘤干性的关键机制.
FOSL1,ALDH1和TRPM7是质瘤的潜在诊断标记物和治疗点.

关键词:

在FOSL1中使用.质瘤是一种质瘤.瘤干细胞是瘤的干细胞.在STAT3中,我们可以使用STAT3.信号通道的信号通道.TRPM7 TRPM7 是一个很好的方法.

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