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通过激活p65/NF-κB信号通路并诱导免疫抑制微环境,CSF3促进结直肠癌的进展

Junfeng Xu¹, Na Li², Hui Xie³

¹Senior Department of Gastroenterology, The First Medical Center of Chinese PLA General Hospital, Beijing 100853, PR China.

Translational oncology

|February 10, 2025

概括

殖民地刺激因子3 (CSF3) 通过激活NF-κB通路促进结直肠癌 (CRC). 沉默CSF3抑制瘤生长并增强抗瘤免疫力,这表明CSF3是CRC的治疗点.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

殖民地刺激因子3 (CSF3) 是一种细胞因子,参与髓状细胞发育和炎症.
目前尚不清楚CSF3在结直肠癌 (CRC) 发病和进展中的具体作用.

研究的目的:

调查CSF3在结直肠癌 (CRC) 的功能意义.
阐明CSF3在CRC中的作用背后的分子机制.
评估CSF3作为CRC的潜在治疗点.

主要方法:

在CRC组织和细胞中,使用qRT-PCR,西斑和IHC.量化了CSF3表达.
在体外和体外测试评估了CSF3对CRC细胞表型和瘤生长的影响.
免疫沉证实了CSF3对IκBα泛化和NF-κB通路激活的影响.

主要成果:

在CRC组织中,CSF3过度表达,与患者存活率较差相关.
沉默CSF3减少了CRC细胞的增殖,迁移和殖民地形成,同时增加了亡.
在体内,CSF3抑制导致瘤生长减少,并调节瘤免疫微环境,促进抗瘤反应.

结论:

CSF3通过通过p65酸化和IκBα无化激活NF-κB信号通路来促进CRC发育和转移.
在调节瘤微环境和CRC中的免疫透中,CSF3起着至关重要的作用.
在抑制CRC进展和转移方面,CSF3是一个有前途的治疗标.

关键词:

在 CSF3 中,CSF3 提供了更多信息.结肠直肠癌是一种癌症.瘤微环境是一个微环境.在Ubiquitination中使用.p65/NF-κB 信号传输方式

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