ArticleCell death & disease2026
Identification of PRRG1 as a possible molecular target of pancreatic cancer.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
In this study, we investigated the expression patterns, biological functions, and molecular mechanisms of Proline-rich γ-carboxylated Gla protein 1 (PRRG1) in pancreatic cancer pathogenesis. Our bioinformatics analysis revealed that PRRG1 expression is markedly upregulated in human PC tissues compared to normal pancreatic tissues, with elevated levels significantly correlating with poor prognosis and advanced histological grade. We verified the high expression of PRRG1 in pancreatic cancer tissue specimens and pancreatic cancer cell lines. Using established PC cell lines (CFPAC-1 and PATU-8988T), we demonstrated that shRNA-mediated PRRG1 silencing effectively suppressed malignant phenotypes, including cell viability, proliferation, migration, and invasion in vitro. Conversely, lentivirus-induced PRRG1 overexpression enhanced these oncogenic behaviors. RNA-sequencing analysis identified the PI3K-Akt signaling pathway as a key downstream effector of PRRG1, with pathway activation status directly correlating with PRRG1 expression levels. Mechanistically, we identified KLF4 as a critical transcription factor binding to the PRRG1 promoter region. In vivo, PRRG1 knockdown inhibited tumor growth and PI3K-Akt activation in subcutaneous xenograft models, while PRRG1 overexpression accelerated tumor progression. Low-dose warfarin (2uM) decreased the levels of PRRG1 and GAS6/AXL axis, markedly suppressed the pro-tumorigenic effects driven by PRRG1 overexpression in vitro and in vivo. Notably, single-cell sequencing analysis revealing high PRRG1 expression specifically in PC epithelial cells. These PRRG1-positive epithelial cells not only exhibited enriched PI3K-Akt signaling activity but also showed significant interactions with macrophages and endothelial cells, which were further validated in immunocompetent models in vivo. However, warfarin effectively reversed the PRRG1 overexpression-driven changes in TME. In conclusion, our findings establish PRRG1 as a key driver of pancreatic cancer progression through PI3K/Akt pathway activation and KLF4-mediated transcriptional regulation. PRRG1 facilitates the establishment of a pro-tumorigenic and immunosuppressive TME in PC. Low-dose warfarin significantly suppressed the pro-tumorigenic effects and the PRRG1 overexpression-driven alterations in the tumor immune microenvironment.
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