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BRAF调节circPSD3/miR-526b/RAP2A轴,以阻碍乳头甲状腺癌的进展

Chuang Li¹, Xiaojuan Zhao¹, Jingge Zhao²

¹Department of Ultrasound, Henan Provincial People's Hospital, No. 7 Weiwu Road, Jinshui District, Zhengzhou, Henan, 450000, China.

BMC molecular and cell biology

|January 21, 2025

概括

循环RNA PSD3 (circPSD3) 通过通过海绵化miR-526b对RAP2A进行上调来促进乳头甲状腺癌 (PTC) 的进展. 过度表达BRAF会抑制circPSD3,从而阻碍PTC的发展.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

乳头甲状腺癌 (PTC) 是一种普遍存在的恶性瘤.
BRAF^V600E突变是PTC的一个关键事件.
循环RNAPSD3 (circPSD3) 在PTC中的作用及其与BRAF的关系仍然不清楚.

研究的目的:

为了研究circPSD3在PTC中的生物功能作用.
阐明 circPSD3 在 PTC 发病过程中的分子机制.
在PTC中探索circPSD3和BRAF之间的关系.

主要方法:

定量实时PCR (RT-qPCR) 用于基因表达分析.
细胞活力,增殖,亡,迁移和入侵试验.
路西法雷斯记者测定和体内异种移植实验.

主要成果:

circPSD3在PTC中高度表达,促进细胞生长,迁移,并抑制细胞亡.
circPSD3通过海绵化miR-526b来调节RAP2A,这一机制通过miR-526b抑制而逆转.
在PTC中对BRAF进行下调;BRAF过度表达通过降低circPSD3和RAP2A的调节,并通过上调 miR-526b来抑制PTC进展.

结论:

circPSD3通过circPSD3/miR-526b/RAP2A路径驱动PTC的进展.
通过抑制circPSD3的表达,BRAF在PTC中起到瘤抑制作用.
针对circPSD3/miR-526b/RAP2A轴或BRAF调制提供了PTC潜在的治疗策略.

关键词:

机理机制机理机制乳头甲状腺癌是一种乳头甲状腺癌.病变的发生和发病.环绕RNAss 的时间.这就是miRNAs.

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