锡利宾对前列腺癌中托雷林诱导的骨代谢异常的影响,基于基于TMT的蛋白质组学揭示
Jianhui Li1, Xuejiao Lv1, Ying Jiang1,2
1Heilongjiang University of Chinese Medicine, Harbin, China.
PloS one
|January 29, 2026
概括
SB和TRP抑制LNCaP细胞的增殖,迁移和入侵,而联合治疗更有效. 通过IL-17信号通路和特定蛋白质,SB可以调节TRP诱导的骨代谢异常.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 蛋白质组学是指蛋白质组学.
背景情况:
- 前列腺癌骨转移是一个重大的临床挑战.
- 了解前列腺癌骨代谢异常背后的分子机制对于开发有效疗法至关重要.
研究的目的:
- 研究SB对LNCaP细胞中TRP诱导的骨代谢异常的作用机制.
- 确定参与这些过程的关键分子标.
主要方法:
- 细胞增殖,迁移和入侵分析 (CCK-8,Transwell).
- 使用Tandem Mass Tag (TMT) 标签和LC-MS/MS进行蛋白质组学分析.
- 对差异表达蛋白质 (DEP) 的生物信息学分析.
- 关键目标的西点验证.
主要成果:
- SB和TRP证明了依赖于剂量和时间的LNCaP细胞增殖,迁移和入侵的抑制,在组合中观察到协同效应.
- 蛋白质组学发现了大量的DEP,组合组中有524个DEP.
- 生物信息学分析显示,在SB和组合组中,IL-17信号通路的丰富,而TRP和组合组显示在循环带动和阿佩林信号通路的丰富.
结论:
- 通过IL-17信号通路,SB可以调节LNCaP细胞中TRP诱导的骨代谢异常.
- 包括p-ERK2,RELA,HSP90B1,GNAI1和GNAI3在内的关键差异表达蛋白 (DEPs) 被确定为潜在的标.
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