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由NAT10介导的ac4C乙化驱动的m6通过YTHDC1-LDHA/PFKM参与的修饰调节糖解并促进骨髓瘤

Zhongting Mei¹, Zhihua Shen^2,3, Jiaying Pu^2,3

¹Department of Pharmacology, (The State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, China.

Cell communication and signaling : CCS

|January 17, 2024

概括

酶NAT10调节RNAN4-乙基 (ac4C) 修饰,影响癌症的进展. 抑制NAT10可以提高RNA N6-甲基氨酸 (m⁶A) 的水平,抑制骨髓瘤的生长和糖解.

科学领域:

生物化学生物化学
分子生物学分子生物学
在瘤学瘤学.

背景情况:

像m6A这样的动态RNA修饰在癌症中至关重要,但上游调节者仍未得到充分探索.
研究了N4-乙基提丁 (ac4C) 乙化酶NAT10在骨髓瘤中的作用及其与m⁶A修饰的联系.

研究的目的:

为了研究NAT10的作用,一个N4-乙基胺 (ac4C) 乙化酶,在骨髓瘤.
阐明NAT10,m6A修饰和癌细胞代谢之间的联系.

主要方法:

在骨髓瘤组织中评估NAT10表达.
在骨髓瘤细胞中进行了NAT10淘汰实验.
分析了m6A水平,mRNA稳定性和蛋白质翻译.
研究了YTHDC1在调节糖解相关基因 (PFKM,LDHA) 中的作用.
在体内瘤模型和细胞实验中用于验证.

主要成果:

在骨髓瘤中,NAT10的表达很高,其降低抑制了瘤的生长,迁移和入侵.
抑制NAT10会增加m6A含量,并降低YTHDC1mRNA的稳定性和翻译.
YTHDC1在PFKM和LDHAmRNA上识别了m6A,抑制了糖解.
在体内和体外,YTHDC1在一定程度上挽救了NAT10倒退的影响.

结论:

由NAT10驱动的ac4C修饰积极调节癌细胞糖解.
在骨髓瘤进展中发现了一种新的信号轴 (NAT10/ac4C-YTHDC1/m6A-LDHA/PFKM).
向NAT10可能通过调节RNA修饰和代谢来为骨髓瘤提供治疗策略.

关键词:

葡萄糖溶解是什么? 葡萄糖溶解 LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA LDHA 是是是是是是是是是是是是是是是在 NAT10 中,NAT10 包含了NAT10.骨质肉瘤骨质肉瘤是什么这就是PFKM.在 YTHDC1 中.在 ac4C 乙化过程中,m6A甲基化的情况.

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