FADS3通过脂质滴/TGF-β受体轴桥梁代谢重编程和上皮质可塑性推动了CcRCC的进展
Kai Sun1, Hongju Ling1, Fan Peng1
1Urology department, Shandong Province Hospital, Shandong University, Jinan, China.
International journal of surgery (London, England)
|November 28, 2025
概括
脂肪酸脱酶3 (FADS3) 通过改变脂肪酸代谢和上皮-介质酶过渡 (EMT) 来促进清细胞细胞癌 (ccRCC) 的进展. FADS3可以作为ccRCC的诊断和预后生物标志物.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 代谢研究研究 代谢研究
背景情况:
- 在清细胞细胞癌 (ccRCC) 中异常的脂质滴积累与代谢重编程有关.
- 连接代谢重编程与ccRCC瘤进展的精确机制需要进一步研究.
研究的目的:
- 在ccRCC中阐明脂肪酸代谢和瘤进展之间的关系.
- 确定ccRCC进展中的关键调节蛋白及其潜在机制.
主要方法:
- 利用多种omics技术来分析脂肪酸代谢和瘤进展.
- 研究了蛋白质在瘤进展和脂肪酸代谢中的作用 in vivo 和 in vitro.
- 采用共免疫沉和质谱法来剖析调节性蛋白质机制.
主要成果:
- 在ccRCC中,脂肪酸脱酶3 (FADS3) 被确定为连接脂肪酸代谢和上皮-介质细胞过渡 (EMT) 的关键调节器.
- 在ccRCC中FADS3上调与晚期临床阶段,不良预后和免疫调节相关.
- 通过TGF-β信号传递,FADS3促进ccRCC的扩散,EMT,苏尼替尼抗性,并通过TGF-β信号传递诱导脂肪酸合成和脂质滴积累.
结论:
- 在调节ccRCC脂肪酸代谢和瘤进展方面,FADS3起到关键的中间蛋白质作用.
- FADS3显示出作为ccRCC的诊断和预后生物标志物的潜力.
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