
The study findings demonstrate the gradual decrease of S100P binding partner (S100PBP) during pancreatic ductal adenocarcinomas (PDAC) progression. Loss of S100PBP prompts oncogenic transformation in pancreatic cells, causing gene alterations influencing cytoskeleton, motility, and survival. S100P overexpression reduces S100PBP levels via complex interactions, and KrasG12D activation suppresses S100PBP, countered by low-dose HDAC inhibitor MS-275. High S100P and low S100PBP expression correlate with poor prognosis in PDAC patients. This establishes S100PBP as a potential tumor suppressor gene, its regulation intricately linked with KrasG12D and epigenetic factors.
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