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FOXA1驱动的通路加剧了结直肠癌中放射治疗诱导的损伤

Minhai Zhang¹, Jingyuan Yang², Guodong Liang¹

¹Department of Emergency Medicine, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou 510080, China.

International immunopharmacology

|March 12, 2024

概括

叉头盒A1 (FOXA1) 通过增加氧化应激和亡,加剧放射治疗引起的急性损伤 (AKI). 这通过FOXA1/ITCH/TXNIP通路发生,该通路激活NLRP3炎症体,导致损伤.

科学领域:

分子生物学分子生物学
在瘤学瘤学.
腎臟病學 (nephrology) 是一種醫學專業.

背景情况:

叉头盒A1 (FOXA1) 与各种癌症有关,但其在急性损伤 (AKI) 中的作用尚不清楚.
结直肠癌的放射治疗可以诱导AKI,强调需要识别导致的分子机制.
了解FOXA1在辐射诱导的AKI中的作用,对于开发有针对性的治疗策略至关重要.

研究的目的:

在结直肠癌模型中研究FOXA1在放射治疗诱导的AKI中的作用.
阐明参与AKI病原发生的FOXA1的下游监管目标.
探索FOXA1/ITCH/TXNIP轴及其对氧化应激和NLRP3炎症酶激活的影响.

主要方法:

建立一个辐射诱导的AKI小鼠模型,并使用转录组分析和qPCR来评估FOXA1表达.
通过lentiviral介导的FOXA1沉默,以评估其对细胞和AKI模型中亡的影响.
生物信息学,ChIP试验,共免疫沉和双露西法酶记者试验,以确定FOXA1-ITCH-TXNIP相互作用及其对氧化应激和NLRP3炎症酶激活的功能影响.

主要成果:

辐射诱导AKI的小鼠的脏组织和受损的HK-2细胞中,FOXA1的表达显著上调.
福克斯A1抑制了E3泛基因酶ITCH的转录,导致 tubular 细胞亡和组织损伤的增加.
在AKI小鼠模型中,ITCH介导的TXNIP泛基化抑制了氧化应激和NLRP3炎症酶激活.

结论:

福克斯A1在加剧放射治疗诱导的AKI中发挥着关键作用.
FOXA1/ITCH/TXNIP轴促进氧化应激,细胞亡和NLRP3炎症酶激活,有助于AKI.
向FOXA1通路可能为减轻放射治疗引起的损伤提供治疗策略.

关键词:

急性损伤是什么?急性损伤是什么?我们的FOXA1A1 吃了一下,吃了一下.在NLRP3炎症酶体中,NLRP3炎症氧化应激是一种氧化应激.辐射疗法辐射疗法这是直肠癌.在TXNIP中,您可以使用TXNIP.

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