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Available4.3
5 reviewsCytoplasmic sequestration of wild-type p53, representing a nonmutational event of p53 activity suppression, is a characteristicphenotype of undifferentiated neuroblastoma (NB); however, the underlying mechanism is yet to be defined. In the present study,we observed that TSPYL5 effectively tethers p53 in the cytoplasm and greatly inhibits its function as a transcription factor.1234567890();,:Mechanistically, the binding of TSPYL5 with G3BP1 enhances G3BP1 Ser149 phosphorylation to drive G3BP1 nuclear membranetranslocation, which recruits more p53 for nucleoporin RanBP2 by the formation of the RanBP2-G3BP1-p53 complex. Thus, theaccelerating p53 sumoylation promotes its nuclear export. With this signal pathway, TSPYL5 augments the malignant characteristicsof neuroblastoma cells. Our findings unravel a detailed TSPYL5-driven molecular axis that sheds light on the regulating system ofthe p53 sumoylation-based cytoplasmic sequestration in NB cells, paving the way for the novel therapeutic opportunities for NBcancers by antagonizing TSPYL5 function.Cell Death and Disease (2025) 16:358 ;
4.8
36 reviews