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Apoptosis is implicated as an important mediator of the tumor suppressive function of TGF-β, although this process remains poorly understood. To address this long-standing question, we dissected the tumor suppressive action of TGF-β in naïve pancreatic ductal adenocarcinoma (PDA) cells. Here we show that TGF-β/Smad4 signaling triggers an EMT in Kras-mutant pancreatic progenitor cells but turns this process into a trigger of apoptosis by converting the progenitor cell transcription factor Sox4 from an enforcer of epithelial progenitor identity into an activator of apoptosis. This occurs as a result of the EMT-linked repression of the endodermal master regulator Klf5, which cooperates with Sox4 to promote epithelial progenitor identity, and loss of which unmasks a latent apoptotic transcriptional program driven by Sox4. By losing Smad4, Kras-mutant PDA cells avoid this fate and instead use Sox4 as a TGF-β-dependent enforcer of the epithelial progenitor cell state. Overall design: In this study, 16 RNA-Seq samples and 6 ChIP-Seq samples are included."],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Mus musculus","description":"TGF-β Tumor Suppression Through A Lethal EMT","dates":{"last_updated":"2025-09-24","first_public":"2016-10-10"},"accession":"PRJNA292864","cross_references":{"GEO":["GSE72069"],"taxon":["10090"],"PubMed":["26898331"]}}