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MiR-494通过G6pc向诱导新陈代谢变化,并在肝细胞癌中调节索拉芬尼的反应

Christian Bergamini¹, Ilaria Leoni^2,3, Nicola Rizzardi¹

¹Department of Pharmacy and Biotechnology, University of Bologna, 40126, Bologna, Italy.

Journal of experimental & clinical cancer research : CR

|June 10, 2023

概括

微RNA-494 (miR-494) 在肝细胞癌 (HCC) 中通过准葡萄糖6-酸酶催化子单元 (G6pc) 来驱动代谢重编程. 升高的miR-494表明sorafenib耐药性,并表明组合疗法的潜力.

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:

代谢重编程是癌症的标志,特别是在肝细胞癌 (HCC) 发育的早期.
目前先进的HCC治疗缺乏有效的循环生物标志物来分层患者.
对于生物标志物和新的治疗策略来克服HCC中药物耐药性的急需.

研究的目的:

研究miR-494在HCC代谢重编程中的作用.
为了确定基于miRNA的新型治疗组合,用于HCC.
评估miR-494作为一种潜在的循环生物标志物,用于HCC治疗反应.

主要方法:

生物信息学分析以确定miR-494的代谢标.
定量PCR (QPCR) 用于测量HCC患者和模型中的葡萄糖6-酸酶催化子单元 (G6pc).
功能性测试用于评估G6pc向,代谢变化,线粒体功能障碍和ROS产生.
实时成像评估miR-494/G6pc轴对HCC细胞生长的影响.
在HCC患者和接受索拉芬尼布治疗的老鼠中测定循环中的miR-494水平.

主要成果:

通过向G6pc和激活HIF-1A通路,MiR-494促进了HCC细胞中的糖溶性表型.
miR-494/G6pc轴促进了代谢可塑性,导致糖原和脂质的积累,增强了细胞生存.
高血清miR-494水平与HCC模型和患者的索拉芬尼抗药性相关.
与antagomiR-494和sorafenib或2-deoxy-glucose的联合治疗显示出增强的抗癌作用.

结论:

miR-494/G6pc轴对癌细胞代谢重新连接至关重要,并且与HCC的预后不佳有关.
在HCC中,MiR-494显示为索拉费尼布响应的预测生物标志物.
在HCC中,MiR-494是组合策略的潜在治疗标,特别是在免疫治疗不合格的患者中.

关键词:

生物标志物生物标志物 G6pccc 在线观看在HCC中,HCC是HCC,HCC是HCC.代谢过程中的代谢.索拉费尼布 (Sorafenib) 是一种在 miR-494 里面,你会看到 miR-494.这是一个微型RNA.

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