ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
SP1-Mediated Glycolytic Reprogramming Promotes Tumorigenesis and Progression in Pancreatic Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- 5MPN effectively targets PFKFB4 and inhibits the glucose metabolism process and invasion of glioblastoma.Translational cancer research · 2025Article
- SP1-Mediated Glycolytic Reprogramming Promotes Tumorigenesis and Progression in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
22 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy, commonly progressing from pancreatic intraepithelial neoplasia (PanIN). However, the molecular alterations in PanIN lesions and their contribution to PDAC progression remain poorly defined. Here, using laser capture microdissection-based proteomics of patient tissues, early metabolic remodeling and upregulation of the transcriptional factor specificity protein 1 (SP1) in PanIN lesions are identified, which persisted into the PDAC stage. That SP1 overexpression promoted PDAC proliferation is demonstrated in patient-derived organoid xenograft models (PDOXs), while deletion of Sp1 inhibited tumorigenesis and progression in a transgenic mouse model of PDAC (Kras
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