促炎细胞因子
炎症
NF-κB
癌症研究
癌变
转录因子
血管生成
癌症
免疫系统
免疫学
发病机制
NFKB1型
生物
医学
基因
遗传学
作者
Hongmei Mao,Xiaocui Zhao,Shao‐Cong Sun
标识
DOI:10.1038/s41423-025-01310-w
摘要
Abstract Nuclear factor-κB (NF-κB) is a family of transcription factors that transactivates genes associated with a wide range of biological processes, including immune responses, inflammation, cell growth and survival. Dysregulated NF-κB activation contributes to acute and chronic inflammatory disorders, mostly through the aberrant induction of genes encoding proinflammatory factors and metabolic disorders. Abnormal NF-κB activation also influences the development and stability of regulatory T cells, contributing to the pathogenesis of autoimmune disorders. Given the critical role of inflammation in promoting oncogenesis, the proinflammatory role of NF-κB is also linked to cancer development. In addition, aberrant NF-κB activation contributes to uncontrolled tumor cell proliferation, survival, metabolism, metastasis, tumor angiogenesis and therapy resistance. These pathological functions of NF-κB highlight its potential as a therapeutic target for both inflammatory diseases and cancer. In this review, we summarize recent findings regarding the role of NF-κB in these pathological processes and discuss the underlying mechanisms. We also explore potential therapeutic strategies aimed at targeting the NF-κB pathway for disease treatment, along with an analysis of possible challenges.
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