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PARP14有助于瘤相关的巨细胞表型的发展

Isotta Sturniolo^1,2, Csongor Váróczy^1,3, Zsolt Regdon¹

¹Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.

International journal of molecular sciences

|April 13, 2024

概括

聚ADP-ribose) 聚合酶 (PARP) 酶,特别是PARP14,在重编程巨细胞转化为瘤相关巨细胞 (TAMs) 中至关重要. 抑制PARP14抑制TAM的发展,提供一种潜在的抗癌策略来增强免疫反应.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
分子生物学分子生物学

背景情况:

癌症重编程巨细胞 (MΦs) 成为促进瘤的瘤相关巨细胞 (TAMs),类似于抗炎M2表型.
聚 ((ADP-ribose) 聚合酶 (PARP) 酶影响MΦ生物学,但它们在TAM发育中的作用尚未被探索.

研究的目的:

研究PARP酶,特别是PARP14在巨细胞对TAM表型的分化中的作用.
评估PARP抑制剂 (PARPis) 作为重编程TAM和增强抗癌免疫力的策略的潜力.

主要方法:

用PARPis (PJ34和MCD113) 治疗原发性小鼠MΦs,人类THP-1单细胞MΦs和原发性人类单细胞衍生的MΦs.
分析M2标记基因表达和MΦ差异化在PARP14淘汰赛 (KO) 小鼠.
利用TAM极化的小鼠和人类模型,包括与乳腺癌细胞共培养的球体.

主要成果:

PARP 抑制剂 (PJ34,MCD113) 和 PARP14 KO 抑制了 M2 标记基因表达.
帕尔P14缺乏限制了MΦ分化到M2细胞.
在小鼠和人类模型中,PARPis和PARP14 KO减少了TAM两极分化,在治疗的球状体中观察到癌细胞亡的增加.
鉴定出利波卡林-2,MIF和PAI-1是依赖ADP-ribosylation的TAM分化的潜在媒介.

结论:

在TAM分化中,PARP14起着重要的作用.
抑制PARP14有效抑制TAM两极分化,并促进癌细胞的亡.
准PARP14是一种有希望的抗癌策略,可以重编程TAM并增强抗癌免疫反应.

关键词:

在ADP-ribosylation过程中.在 PARP14 中,我们可以使用 PARP14 乳腺癌乳腺癌乳腺癌巨细胞是一个巨细胞.

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