康迪塞激活自抑制FGF9-诱导的TM3小鼠雷迪格原始细胞的增殖
Su-Zhen Wu1, Yu-Yan Lan2, Chin-Ying Chen3
1Department of Anesthesiology, Chi Mei Medical Center of Liouying, Tainan, Taiwan, R.O.C.
Cancer genomics & proteomics
|October 28, 2024
概括
源自Cordyceps sinensis的 Cordycepin,通过激活自,而不是亡,诱导FGF9治疗的TM3 Leydig细胞中的细胞死亡. 这一发现为与莱迪格细胞相关的疾病提供了一种新的治疗策略.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 纤维细胞生长因子9 (FGF9) 促进莱迪格细胞的增殖和瘤发生.
- 来自Cordyceps sinensis的Cordycepin通过亡和/或自已知具有抗瘤作用.
- FGF9刺激TM3小鼠莱迪格前代细胞中的增殖.
研究的目的:
- 为了研究cordycepin对FGF9治疗的TM3细胞增殖的影响.
- 为了确定cordycepin是否通过apoptosis和/或自在FGF9治疗的TM3细胞中诱导细胞死亡.
主要方法:
- TM3细胞被用皮质素和FGF9.9治疗.
- 采用了流细胞计,免疫光学和西部涂抹.
- 分析了细胞死亡机制.
主要成果:
- 在FGF9治疗期间,康迪塞宾降低了TM3细胞活力和殖民地形成.
- 亡标志物没有显著改变.
- 通过LC3-II上调表示的自被激活.
- 自抑制逆转了皮素诱导的细胞死亡.
结论:
- 科尔迪塞宾在FGF9治疗的TM3细胞中诱导细胞死亡,主要是通过自活化.
- 这些发现强调了自作为cordycepin在莱迪格细胞中的作用的关键机制.
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