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METTL16促进糖溶性代谢重编程和结直肠癌的进展

Wei Wei^1,2, Zhong-Yuan Zhang³, Bin Shi⁴

¹Department of Laboratory Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.

Journal of experimental & clinical cancer research : CR

|June 20, 2023

概括

METTL16/SOGA1/PDK4轴通过增强糖解驱动着结直肠癌 (CRC) 的进展. 针对这种途径为CRC患者提供了一个有前途的治疗策略.

科学领域:

分子瘤学分子瘤学
癌症新陈代谢癌症新陈代谢
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

糖溶解是癌症的关键过程,促进瘤的开始和进展.
在癌症糖解中N6-甲基亚丁素 (m6A) 修饰的作用在很大程度上仍未被探索.
这项研究研究了m6A甲基转移酶METTL16在糖溶性代谢和结直肠癌 (CRC) 进展中的功能.

研究的目的:

探索METTL16在糖溶性代谢中的生物功能.
阐明METTL16在结直肠癌 (CRC) 进展中的作用.
揭示了CRC病原发生的新型机制.

主要方法:

生物信息学和免疫组织化学 (IHC) 用于评估METTL16表达和预后价值.
在体外和体内试验分析了METTL16在CRC进展中的功能.
糖溶性代谢试验,RNA免疫沉降 (RIP),共免疫沉降 (Co-IP) 和RNA下拉试验阐明了分子机制.

主要成果:

METTL16直接针对自性葡萄糖抑制剂 (SOGA1),通过IGF2BP1.1增强其表达和mRNA稳定性.
SOGA1促进AMPK的无处不在,抑制其活性,并上调pyruvate dehydrogenase kinase 4 (PDK4),这是葡萄糖代谢的关键调节者.
METTL16表达与SOGA1和PDK4正相关,并且与CRC患者的预后不佳有关.

结论:

METTL16/SOGA1/PDK4轴是糖解和结直肠癌进展的关键驱动因素.
这一轴代表着结直肠癌 (CRC) 的一个有前途的治疗标.

关键词:

结肠直肠癌是一种癌症.在METTL16中,METTL16是METTL16中的一个.在PDK4中使用PDK4.在SOGA1中,它是SOGA1.m6A 一个很好的.

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