BUD23通过影响PPAR信号通路来促进细胞增殖能力:来自在线数据集和细胞实验的证据
Tao Huang1, Binbin Jiao2, Zhenkai Luo3
1Department of Urology, The First Affiliated Hospital of Nanjing Medical University, No. 300, Guangzhou Road, Nanjing, 210029, China.
Discover oncology
|December 5, 2024
概括
这项研究表明,BUD23的高表达与侵袭性前列腺癌和较差的生存率相关. 向BUD23可能通过调节氧酶增殖器激活受体 (PPARs) 来抑制瘤生长.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症基因组学 癌症基因组学
背景情况:
- 前列腺癌是一个重要的全球健康问题,具有多因素的病因.
- 过氧酶增殖器激活受体 (PPAR) 在前列腺癌中的作用尚未完全理解.
- 研究新的生物标志物和治疗点对于改善患者的治疗结果至关重要.
研究的目的:
- 阐明PPARs在前列腺癌进展中的作用.
- 为了确定前列腺癌的预后生物标志物.
- 探索前列腺癌中BUD23和PPAR信号之间的关系.
主要方法:
- 癌症基因组图谱 (TCGA) 转录组数据的分析.
- 基因组丰富分析 (GSEA),基因本体学 (GO) 和KEGG通路分析.
- 使用考克斯回归和LASSO分析构建预后模型.
- 使用基于细胞的测试 (qPCR,CCK-8,EDU) 和西式涂抹的功能验证.
主要成果:
- 在高和低的PPAR表达群体之间观察到不同的免疫微环境和HLA基因表达特征.
- 一个预后模型将BUD23确定为与患者存活相关的关键基因.
- 增加的BUD23表达与晚期病理阶段,结节转移和更高的格里森分数相关.
- BUD23敲击抑制了前列腺癌细胞的增殖,并降低了PPAR-α,PPAR-β和PPAR-γ蛋白水平.
结论:
- PPARs在前列腺癌进展中发挥着独特的作用,并代表潜在的治疗点.
- BUD23是一种潜在的预后生物标志物,与侵袭性疾病和生存相关.
- 准BUD23可能通过调节前列腺癌中的PPAR信号来抑制瘤生长.
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