Phosphatidylinositol glycan anchor biosynthesis class N (PIGN) has been linked to the suppression of chromosomal instability. The spindle assembly checkpoint complex is responsible for proper chromosome segregation during mitosis to prevent chromosomal instability. In this study, the novel role of PIGN as a regulator of the spindle assembly checkpoint was unveiled in leukemic patient cells and cell lines. Transient downregulation or ablation of PIGN resulted in impaired mitotic checkpoint activation due to the dysregulated expression of spindle assembly checkpoint-related proteins including MAD1, MAD2, BUBR1, and MPS1. Moreover, ectopic overexpression of PIGN restored the expression of MAD2. PIGN regulated the spindle assembly checkpoint by forming a complex with the spindle assembly checkpoint proteins MAD1, MAD2, and the mitotic kinase MPS1. Thus, PIGN could play a vital role in the spindle assembly checkpoint to suppress chromosomal instability associated with leukemic transformation and progression.

磷脂酰肌醇聚糖锚定生物合成 N 类 (PIGN) 与抑制染色体不稳定性有关。纺锤体组装检查点复合体负责在有丝分裂过程中进行适当的染色体分离，以防止染色体不稳定。在这项研究中，PIGN 作为纺锤体组装检查点的调节剂的新作用在白血病患者细胞和细胞系中被揭示。由于纺锤体组装检查点相关蛋白（包括 MAD1、MAD2、BUBR1 和 MPS1）的表达失调，PIGN 的瞬时下调或消融导致有丝分裂检查点激活受损。此外，PIGN的异位过表达恢复了MAD2的表达。PIGN 通过与纺锤体组装检查点蛋白 MAD1、MAD2 和有丝分裂激酶 MPS1 形成复合物来调节纺锤体组装检查点。