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通过控制替代拼接,RAVER1阻碍了致命的EMT,并通过控制替代拼接来调节miR/RISC活动
Alice Wedler1, Nadine Bley1, Markus Glaß1
1Institute of Molecular Medicine, Section for Molecular Cell Biology, Faculty of Medicine, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Nucleic acids research
|February 1, 2024
概括
在癌症中,RAVER1蛋白控制替代拼接 (AS),促进瘤生长和上皮-介质细胞转换 (EMT). 它调节miR/RISC通路,影响基因表达并限制致命的EMT.
科学领域:
- 分子生物学分子生物学
- 癌症生物学 癌症生物学
- 在RNA分离过程中.
背景情况:
- 众所周知,替代拼接的蛋白质调节器RAVER1与聚皮里米丁通道结合蛋白 (PTBPs) 合作.
- 它在癌细胞命运中的特定作用及其在PTBP合作之外的更广泛功能尚未完全理解.
研究的目的:
- 为了研究RAVER1在控制癌细胞模型中的替代拼接 (AS) 中的作用.
- 阐明RAVER1在瘤生长中的功能,上皮细胞-介质细胞转换 (EMT) 和微RNA/RNA诱导的沉默复合体 (miR/RISC) 途径.
主要方法:
- 在癌细胞模型中进行全面的拼接分析.
- 蛋白质关联研究以确定相互作用的拼接调节器.
- 研究RAVER1对miR/RISC通路和基因表达的影响.
主要成果:
- 拉维尔1表现出一种亲瘤作用,促进瘤生长和EMT.
- RAVER1调节miR/RISC通路中的AS事件,包括miR/RISC复合体形成必不可少的TNRC6蛋白中的GW丰富基因.
- 破坏RAVER1会损害miR/RISC活动,导致基因表达放松调节,并促进TGFB驱动的EMT.
结论:
- 在miR/RISC路径中,RAVER1是AS的关键调节器,确保miR/RISC效应器的正确功能.
- RAVER1的活动对于平衡TGFB信号和防止TGFB诱导的致命EMT至关重要.
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