S100PBP is regulated by mutated KRAS and plays a tumour suppressor role in pancreatic cancer.

ABSTRACT: We have previously shown that expression of S100PBP, an S100P binding partner, gradually decreases during progression of pancreatic ductal adenocarcinomas (PDAC). Here, we show that loss of S100PBP leads to oncogenic transformation of pancreatic cells; after deregulation of S100PBP expression, both in silico and in vitro analyses highlighted alterations of genes known to modulate cytoskeleton, cell motility and survival. Overexpression of S100P reduced S100PBP expression, while co-immunoprecipitation indicated the interaction of S100P with S100PBP-p53-ubiquitin protein complex, likely causing S100PBP degradation. The doxycycline-induced Kras^G12D activation resulted in decreased S100PBP levels, while low-dose treatment with HDAC inhibitor MS-275 rescued its expression in both hum

SUBMITTER: Srivastava K 

PROVIDER: S-EPMC10638088 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature