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

doi:10.16352/j.issn.1001-6325.2026.06.0772

Abstract

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

CLC Number:

Q253

GU Rao, LI Weiqian, WANG Fang, YU Jia^*. Effects of NAT10 on the cell cycle and apoptosis of 32D cells[J]. Basic & Clinical Medicine, 2026, 46(6): 772-776.

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