基础医学与临床 ›› 2026, Vol. 46 ›› Issue (6): 772-776.doi: 10.16352/j.issn.1001-6325.2026.06.0772

• 研究论文 • 上一篇    下一篇

NAT10对32D细胞周期和凋亡的影响

顾娆, 李卫倩, 王芳, 余佳*   

  1. 中国医学科学院北京协和医学院 基础医学研究所 生物化学与分子生物学系 重大疾病共性机制研究全国重点实验室,北京 100005
  • 收稿日期:2026-02-09 修回日期:2026-03-27 出版日期:2026-06-05 发布日期:2026-05-27
  • 通讯作者: *j-yu@ibms.pumc.edu.cn
  • 基金资助:
    国家自然科学基金(92268205)

Effects of NAT10 on the cell cycle and apoptosis of 32D cells

GU Rao, LI Weiqian, WANG Fang, YU Jia*   

  1. State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005,China
  • Received:2026-02-09 Revised:2026-03-27 Online:2026-06-05 Published:2026-05-27
  • Contact: *j-yu@ibms.pumc.edu.cn

摘要: 目的NAT10在小鼠髓系祖细胞系32D细胞中的功能。方法 采用CRISPR/Cas9技术敲除32D细胞中的NAT10基因,通过RT-qPCR、Western blot验证敲除效率。用流式细胞术检测细胞周期分布及细胞凋亡情况,并对实验结果进行统计学分析。结果 成功构建了NAT10敲除的32D细胞模型。与对照组相比,NAT10敲除后32D细胞G1期比例显著下降,S期细胞比例显著升高。同时,早期及晚期凋亡细胞比例显著下降(P<0.05)。结论 NAT10在32D细胞的增殖与存活过程中发挥重要作用,其缺失可激活细胞周期,抑制细胞凋亡,提示NAT10可能参与髓系祖细胞的增殖调控,限制其过度增殖。

关键词: NAT10, 髓系祖细胞, 细胞周期, 细胞凋亡

Abstract: Objective To investigate the function of NAT10 in the mouse myeloid progenitor cell line 32D. Methods The NAT10 gene was knocked out in 32D cells using CRISPR/Cas9 technology, and the knockout efficiency was verified by RT-qPCR and Western blot. Flow cytometry was employed to assess cell cycle distribution and apoptosis, and the experimental results were statistically analyzed. Results A NAT10 knockout 32D cell model was successfully established. Compared with the control group, NAT10 knockout resulted in a marked reduction in the percentage of cells in the G1 phase accompanied by a significant increase in the percentage of cells in the S phase. Meanwhile, the proportion of early and late apoptotic cells was significantly reduced (P<0.05). Conclusions NAT10 plays an important role in the proliferation and survival of 32D cells. Its loss can lead to cell cycle activation and inhibition of apoptosis, suggesting that NAT10 may be involved in the regulation of myeloid progenitor cell growth and in limiting their excessive proliferation.

Key words: NAT10, myeloid progenitor cells, cell cycle, apoptosis

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