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CPSF6通过相分离来调节癌细胞的替代多化和增殖

Susu Liu¹, Runze Wu¹, Liutao Chen¹

¹State Key Laboratory for Biocontrol, Guangdong Province Key Laboratory of Pharmaceutical Functional Genes, Department of Biochemistry, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, P.R. China.

|October 1, 2023

概括

癌细胞通过替代多基化 (APA) 缩短3'未翻译区域 (UTR). 我们发现CPSF6的液态液态相分离 (LLPS),而不是表达水平,驱动癌症中的APA调节,影响细胞增殖.

科学领域:

分子生物学分子生物学
癌症研究癌症研究
细胞生物学细胞生物学

背景情况:

癌细胞经常显示缩短的3'未翻译区域 (UTR) 由于替代多基化 (APA),促进增殖和迁移.
升级的CPSF6通常会延长3' UTRs,与其在瘤中的更高表达形成矛盾,需要对其在癌症中的调节机制进行研究.

研究的目的:

研究CPSF6调节癌细胞中替代多基化 (APA) 切换的机制.
探索CPSF6液体-液体相分离 (LLPS) 在APA调节中的作用及其与癌症进展的关联.

主要方法:

调查了CPSF6通过液态液相分离 (LLPS) 的能力.
研究了CLK2激酶通过酸化对CPSF6LLPS的影响.
评估了减少CPSF6LLPS对细胞循环基因和细胞增殖的3' UTR长度的影响.

主要成果:

CPSF6经历液体-液体相分离 (LLPS),LLPS的升高与偏好的远端多A位点使用相关.
在癌症中升级的CLK2激酶通过酸化破坏CPSF6LLPS.
减少CPSF6LLPS导致细胞循环基因中的3' UTRs缩短,加速细胞增殖.

结论:

通过CPSF6介导的LLPS,而不是其表达水平,对于调节癌细胞中的APA至关重要.
CPSF6 LLPS和CLK2酸化之间的相互作用影响3' UTR动态和癌细胞增殖.

关键词:

科普:分子生物学分子生物学在CP:癌症.在CPSF6中.替代性的多基化.癌症细胞的增殖和扩散.阶段分离的相位分离.酸化的方法是:酸化.

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