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在前列腺癌中,ND630通过调节circKIF18B_003的表达来控制ACACA和脂质重编程
Yu-Peng Wu1,2, Wen-Cai Zheng1,2, Qi Huang1,2
1Department of Urology, Urology Research Institute, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Road, Fuzhou, 350005, China.
Journal of translational medicine
|December 4, 2023
概括
药物ND630通过向circKIF18B_003.3,调节前列腺癌中的脂质代谢和ACACA表达. 这项研究揭示了circKIF18B_003作为前列腺癌治疗的潜在治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- ND630是一种针对ACACA和脂质代谢的新型分子,但其在前列腺癌中的作用尚不清楚.
- KIF18B是一种对前列腺癌进展至关重要的瘤基因,其衍生的circRNA,circKIF18B_003,在瘤中过度表达.
- 这项研究调查了ND630通过cirKIF18B_003调节ACACA和脂质重编程对前列腺癌的影响.
研究的目的:
- 为了确定ND630是否控制前列腺癌中的ACACA和脂质重编程.
- 调查circKIF18B_003在前列腺癌进展中的作用.
- 为了阐明ND630在circKIF18B_003.3.0上的调节机制.
主要方法:
- 定量实时PCR (RT-qPCR) 用于circKIF18B_003表达式分析.
- 细胞测定 (CCK-8,殖民地形成,伤口愈合,Transwell) 和异种移植模型来评估circKIF18B_003的功能.
- RNA免疫沉 (RIP),RNA拉下,和光酶记者试验来探索分子机制,包括circKIF18B_003 miR-370-3p.
主要成果:
- circKIF18B_003 前列腺癌组织中的过度表达与患者的生存率差相关.
- circKIF18B_003的升级增强了前列腺癌细胞的增殖,迁移和入侵.
- circKIF18B_003作为miR-370-3p的海绵,增加ACACA表达和促进恶性表型;这种效应被ACACA下调逆转.
- ND630与多塞塞尔结合使用显著减少瘤生长,这表明它在脂质代谢调节中的作用.
结论:
- 在前列腺癌中,ND630通过调节circKIF18B_003表达来调节ACACA和脂质重编程.
- ND630和circKIF18B_003是前列腺癌的一个有前途的新型治疗点.
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