禁食通过IncRNA PRKCQ-AS1介导的IGF2BPs调节线粒体功能在皮肤状甲状腺癌中
Xiaoping Zhang1,2, Yong Zhong3, Lin Liu3
1Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Zhuhai People's Hospital, Zhuhai hospital Affiliated with Jinan University, Jinan University, 519000, Guangdong, China. zxpkxy@tongji.edu.cn.
Cell death & disease
|December 13, 2023
概括
禁食通过减少细胞糖解和线粒体功能障碍来抑制乳头甲状腺癌 (PTC) 的生长. 这通过lncRNA PRKCQ-AS1发生,该RNA针对IGF2BPs/PRMT7信号通路,为PTC提供了一种新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 代谢途径 代谢途径
- 分子生物学分子生物学
背景情况:
- 禁食在各种癌症中表现出抗瘤特性,包括乳头甲状腺癌 (PTC).
- 连接禁食与PTC抑制的确切机制在很大程度上仍未被探索.
- 了解这些机制对于开发新的治疗策略至关重要.
研究的目的:
- 调查禁食对PTC中的糖解和线粒体功能的影响.
- 确定参与PTC中禁食诱导的代谢变化的关键分子参与者.
- 阐明长非编码RNAPRKCQ-AS1在PTC进展及其通过禁食调节中的作用.
主要方法:
- 在体外和体内研究评估了禁食和模仿禁食饮食 (FMD) 对PTC细胞的影响.
- 对基因和蛋白质表达的分析,包括lncRNA PRKCQ-AS1,IGF2BPs和PRMT7.
- 使用共免疫沉和mRNA表达试验,研究分子相互作用.
主要成果:
- 禁食显著损害葡萄糖分解,并减少PTC细胞中的线粒体功能障碍,无论是体外还是体外.
- 禁食和口炎增加了lncRNA PRKCQ-AS1的表达,这种表达在PTC组织中被下调.
- PRKCQ-AS1与IGF2BPs相互作用,增强PRMT7mRNA,从而调节PTC细胞糖解和线粒体功能,最终抑制瘤生长.
结论:
- 在PTC中,lncRNA PRKCQ-AS1是禁食抗瘤作用的关键下游调解者.
- PRKCQ-AS1/IGF2BPs/PRMT7轴在PTC代谢重编程中发挥着至关重要的作用.
- 这一轴代表了对乳头甲状腺癌的诊断和治疗的有前途的治疗标.
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