Abstract：
BACKGROUND: The nuclear factor kappa B (NF-κB) is a critical pathway that regulates various cellular functions, including immune response, proliferation, growth, and apoptosis. Furthermore, this pathway is tightly regulated to ensure stability in the presence of immunogenic triggers or genotoxic stimuli. The lack of control of the NF-κB pathway can lead to the initiation of different diseases, mainly autoimmune diseases and cancer, including Renal cell carcinoma (RCC). RCC is the most common type of kidney cancer and is characterized by complex genetic composition and elusive molecular mechanisms.
OBJECTIVE: The current review summarizes the mechanism of NF-κB dysregulation in different subtypes of RCC and its impact on pathogenesis.
UNASSIGNED: This review highlights the prominent role of NF-κB in RCC development and progression by driving the expression of multiple genes and interplaying with different pathways, including the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway. In silico analysis of RCC cohorts and molecular studies have revealed that multiple NF-κB members and target genes are dysregulated. The dysregulation includes receptors such as TLR2, signal-transmitting members including RelA, and target genes, for instance, HIF-1α. The lack of effective regulatory mechanisms results in a constitutively active NF-κB pathway, which promotes cancer growth, migration, and survival. In this review, we comprehensively summarize the role of dysregulated NF-κB-related genes in the most common subtypes of RCC, including clear cell RCC (ccRCC), chromophobe RCC (chRCC), and papillary RCC (PRCC).
OBJECTIVE: The current review summarizes the mechanism of NF-κB dysregulation in different subtypes of RCC and its impact on pathogenesis.
UNASSIGNED: This review highlights the prominent role of NF-κB in RCC development and progression by driving the expression of multiple genes and interplaying with different pathways, including the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway. In silico analysis of RCC cohorts and molecular studies have revealed that multiple NF-κB members and target genes are dysregulated. The dysregulation includes receptors such as TLR2, signal-transmitting members including RelA, and target genes, for instance, HIF-1α. The lack of effective regulatory mechanisms results in a constitutively active NF-κB pathway, which promotes cancer growth, migration, and survival. In this review, we comprehensively summarize the role of dysregulated NF-κB-related genes in the most common subtypes of RCC, including clear cell RCC (ccRCC), chromophobe RCC (chRCC), and papillary RCC (PRCC).
摘要：
背景：核因子κB（NF-κB）是调节各种细胞功能的关键途径，包括免疫反应，扩散,增长,和凋亡。此外，该途径受到严格调控,以确保在免疫原性触发因素或遗传毒性刺激存在下的稳定性.缺乏对NF-κB通路的控制可导致不同疾病的开始，主要是自身免疫性疾病和癌症，包括肾细胞癌（RCC）。肾癌是最常见的肾癌类型，其特征是复杂的遗传组成和难以捉摸的分子机制。
目的：综述NF-κB调控异常在不同亚型RCC中的作用机制及其对发病的影响。
■这篇综述通过驱动多个基因的表达和与不同途径的相互作用，突出了NF-κB在RCC发生和进展中的重要作用。包括磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)途径。RCC队列的计算机模拟分析和分子研究表明，多个NF-κB成员和靶基因失调。失调包括受体，如TLR2，信号传递成员，包括RelA，和目标基因，例如,HIF-1α。缺乏有效的调节机制导致组成型活性的NF-κB途径，促进癌症生长，迁移,和生存。在这次审查中,我们全面总结了NF-κB相关基因在RCC最常见亚型中的作用，包括透明细胞RCC(ccRCC)，发色细胞RCC（chRCC），和乳头状RCC（PRCC）。
目的：综述NF-κB调控异常在不同亚型RCC中的作用机制及其对发病的影响。
■这篇综述通过驱动多个基因的表达和与不同途径的相互作用，突出了NF-κB在RCC发生和进展中的重要作用。包括磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)途径。RCC队列的计算机模拟分析和分子研究表明，多个NF-κB成员和靶基因失调。失调包括受体，如TLR2，信号传递成员，包括RelA，和目标基因，例如,HIF-1α。缺乏有效的调节机制导致组成型活性的NF-κB途径，促进癌症生长，迁移,和生存。在这次审查中,我们全面总结了NF-κB相关基因在RCC最常见亚型中的作用，包括透明细胞RCC(ccRCC)，发色细胞RCC（chRCC），和乳头状RCC（PRCC）。
