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在白血病B细胞中,米R-155缺乏和缺氧导致代谢切换

Elena Golovina¹, Tomas Heizer^1,2, Lenka Daumova³

¹Institute of Pathological Physiology, First Faculty of Medicine, Charles University, Prague, Czech Republic.

Cancer cell international

|July 17, 2024

概括

慢性淋巴细胞白血病 (CLL) 细胞中MICRORNA-155 (miR-155) 缺乏会降低细胞的增殖,并在缺氧下增加细胞亡. 这会通过改变基因表达来影响葡萄糖和乳酸代谢.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

缺氧是刺激白血病细胞生长的关键因素.
微RNAs (miRNAs) 在白血病的发展和进展中起着至关重要的作用.
在缺氧下白血病细胞中miRNAs和mRNAs之间的相互作用尚未完全理解.

研究的目的:

研究hsa-miR-155-5p (miR-155) 在低氧条件下对慢性淋巴细胞白血病 (CLL) 细胞的新陈代谢,增殖和mRNA/miRNA网络的影响.
分析miR-155在MEC-1CLL细胞中调节基因表达和细胞过程中的作用.

主要方法:

利用CRISPR/Cas9在人类MEC-1细胞系中删除成熟的miR-155,这是CLL的一个模型.
在低氧条件下评估细胞增殖,细胞周期阶段分布 (S阶段) 和细胞亡.
分析了关键代谢和缺氧相关基因 (EGLN1,GLUT1,GLUT3) 的基因表达.
测量葡萄糖和乳酸盐摄入量,酸盐,ETC和ATP水平.

主要成果:

miR-155缺乏导致MEC-1细胞的增殖减少和S相人口减少,即使在低氧状态下.
低氧与miR-155缺乏结合,导致亡的增加.
基因表达分析显示,miR-155缺乏细胞中EGLN1,GLUT1和GLUT3的显著过度表达.
miR-155缺乏和缺氧增加了葡萄糖和乳酸盐的摄取,同时降低了pyruvate,ETC和ATP水平.

结论:

miR-155缺乏显著影响低氧下CLL细胞的行为,减少增殖和增加亡.
缺少miR-155刺激葡萄糖载体 (GLUT1,GLUT3) 和EGLN1的表达,从而改变葡萄糖和乳酸代谢.
这些发现突显了miR-155在维持低氧环境中的白血病状态中的作用,并表明了潜在的治疗点.

关键词:

乙细胞是B细胞的一个组成部分.这就是CRISPR/Cas9的作用.细胞活力细胞活力基因表达基因表达基因表达氧气过低是因为缺氧.在白血病中,白血病.这是一个小RNARNA.

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