在K562细胞中D-糖诱导的细胞毒性:RBKS依赖的铜恒温和线粒体功能的破坏
Wang Zeying1, Li Houyu1, Yang Zhongbin1
1Department of Biochemistry and Molecular Biology, Baotou Medical College, Baotou, Inner Mongolia, China.
Free radical biology & medicine
|February 6, 2026
概括
D-ribose通过破坏铜恒温和氧化酸化来抑制细胞增殖,揭示了一条新的细胞毒性途径. 这一发现对于理解D-ribose至关重要.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 一种糖糖的D-ribose通过ribokinase (RBKS) 被化成ribose-5-phosphate.
- 尿液D-ribose的升高与2型糖尿病 (T2DM) 和阿尔茨海默病有关.
- 之前对D-ribose细胞毒性的研究集中在糖化上,忽视了其他机制.
研究的目的:
- 为了研究D-ribose除了糖化之外的其他细胞毒性机制.
- 检查D-ribose在K562细胞中的作用,这些细胞表达可诱导的血红蛋白.
主要方法:
- 在K562细胞中使用CCK-8试验来评估细胞增殖.
- 使用RBKS过度表达和淘汰,研究其对细胞增殖和氧化应激的影响.
- 转录组分析 (RNA测序) 和RT-qPCR用于识别差异表达的基因并验证发现.
主要成果:
- D-ribose以剂量和时间依赖的方式抑制了K562细胞的增殖,在分化的细胞中增强了效果.
- 过度表达RBKS促进了增殖并减少了氧化应激.
- D-ribose治疗和RBKS淘汰会降低铜的稳态和线粒体呼吸链基因的调节,导致细胞内自由铜的减少.
结论:
- 一种涉及RBKS-铜-氧化酸化轴的新型细胞毒性机制被确定为D-ribose.
- 这项研究提供了对D-ribose细胞内功能和细胞毒性作用的关键见解.
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