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通过降低ABCC10表达的调节,let-7g使肝癌细胞对5-甲敏感

Yun Chen^1,2,3, Bocheng Zhang^2,3,4,5, Cui Zhong⁶

¹Department of Pharmacy, Hunan Cancer Hospital/The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P. R. China.

Chemical biology & drug design

|December 6, 2023

概括

这项研究表明,let-7g微RNA通过降低ABCC10.10的调节,使肝癌细胞对5-甲 (5-FU) 治疗敏感. 这一发现为克服晚期肝癌中5-FU耐药性的潜在策略提供了机会.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生化学

背景情况:

晚期肝癌患者往往会对5-甲 (5-FU) 治疗产生耐药性,导致结果不佳.
了解5-FU耐药性背后的分子机制对于提高治疗疗效至关重要.

研究的目的:

调查let-7g/ABCC10轴在调节肝癌细胞中5-FU抗性的作用.
探索let-7g作为克服5-FU抗性的潜在治疗点.

主要方法:

建立了一种抗5-FU的肝癌细胞系 (Huh-7/4X).
使用了CCK8,流细胞测量,TUNEL染色,PCR,西部斑点和双露西法酶记者测试.
在实验室和体内使用裸体小鼠模型评估let-7g在5-FU敏感性的作用.

主要成果:

在肝癌细胞中,特别是Huh-7细胞中,let-7g的表达显著下降.
过度表达let-7g抑制了Huh-7/4X细胞活力,诱导G1阶段停止,并促进了细胞亡.
let-7g直接准了ABCC10,降低了其表达,从而增加了对5-FU的敏感性,无论是体外还是体内.

结论:

let-7g通过降低ABCC10的调节作用作为瘤抑制剂,从而使肝癌细胞对5-FU敏感.
-7g/ABCC10轴代表了克服肝癌中5-FU抗性的有前途的治疗标.

关键词:

5 - - 甲酸的使用情况在ABCC10中,ABCC10是ABCC10的位置.药物耐药性耐药性药物耐药性肝细胞癌是肝细胞癌.让-7g成为-7g.

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