S100结合蛋白A8 通过激活NF-κB信号通路,在细胞癌中起到促进瘤的作用
Shu-Hui Wang1, Yan-Jie Xia2, Jing Yu3
1Department of Integrated Traditional Chinese and Western Medicine and Geriatrics, Hongqi Hospital Affiliated to Mudanjiang Medical University, Mudanjiang, Heilongjiang, China.
概括
下调S100结合蛋白A8 (S100A8) 抑制细胞癌 (RCC) 细胞生长,并促进细胞亡. 这通过非激活NF-κB信号通路而发生,这表明S100A8是RCC的潜在治疗标.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 细胞癌 (RCC) 是一种常见的尿生殖系统恶性瘤,起源于管状表皮.
- 确定S100结合蛋白A8 (S100A8) 在RCC组织中表达高,并与癌症发展有关.
- S100A8作为炎症调节因子,参与癌症进展.
研究的目的:
- 调查S100A8在细胞癌的生物行为中的作用.
- 探索潜在的分子机制,包括信号通路和炎症反应,由RCC中S100A8调节.
- 评估S100A8作为细胞癌的潜在治疗标.
主要方法:
- 利用基因表达综合 (GEO) 数据库 (GSE100666) 进行基因表达分析.
- 收集了人类RCC样本和相邻的正常组织,用于西部涂抹和S100A8.8的免疫组织化学分析.
- 在786-O和ACHN RCC细胞系中进行了S100A8过度表达和淘汰,随后进行了MTT和亡试验,并评估了炎症标志物.
主要成果:
- 降低S100A8的调节显著抑制了786-O和ACHN RCC细胞中的增殖和诱导的亡.
- 沉默S100A8导致NF-κB p65的酸化降低,降低了TNF-α,分裂的卡斯帕酶-1和MMP9.9的水平.
- 相反,S100A8上调增加了这些炎症和亡标志物的表达.
结论:
- 通过关闭NF-κB信号通路,S100A8 Knockdown可以抑制RCC的恶性生物特性.
- 这些发现凸显了S100A8作为细胞癌的潜在治疗标.
- 这项研究为S100A8在RCC发病过程中的作用及其与炎症途径的关联提供了新的见解.
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