Journal
SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-98218-y
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Funding
- AA&MDSIF research grant [146818]
- American Cancer Society [124171-IRG-13-043-02]
- NIDA/FDA research grant [P50 DA036107]
- JT Tai & Co Foundation Cancer Research Grant
- Pennsylvania State University College of Medicine research grant
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PIGN, as a regulator of the spindle assembly checkpoint, affects the activation of mitotic checkpoint in leukemic cells, which in turn influences chromosome segregation, suggesting a crucial role in suppressing chromosomal instability associated with leukemia.
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.
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