ArticleGut2024
Pancreatic STAT5 activation promotes Kras
Article in Gut, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- IL-22Rα1 restrains pancreatic injury independently of its C-terminal STAT3-amplifying domain.Journal of cell communication and signaling · 2026Article
- Protease-Activated Receptor-2 as a Proteolytic Rheostat in Colorectal and Pancreatic Cancer: From Mechanism to Biomarker-Guided Therapy.International journal of molecular sciences · 2026Review
- Single-Dose L-Lysine-Induced Pancreatitis Followed by Pancreatic Neoplastic Progression in AdultMethods and protocols · 2026Article
- Liver Kinase B1 in CD11cAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Reinvigorating COTL1Nature cell biology · 2026Article
- Review
- Interruption of cross-communication pathways alters the immune cell signature of pancreatic cancer and decreases tumor growth.Cell communication and signaling : CCS · 2026Article
- Research progress on the etiology and pathogenesis of pancreatic cancer: a narrative review.Frontiers in oncology · 2026Review
- Targeted nanoencapsulation of tunicamycin reduces toxicity while improving its therapeutic effectiveness in pancreatic cancer cells.Molecular therapy. Oncology · 2025Article
- First Report of Trametinib-Nintedanib Combination in KRAS G12D-Mutated Pancreatic Cancer: Efficacy and Fatal Hemorrhagic Complication: A Case Report.Clinical case reports · 2025Article
- SP1-Mediated Glycolytic Reprogramming Promotes Tumorigenesis and Progression in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Prognostic significance of advanced lung cancer inflammation index in resectable pancreatic cancer: A retrospective study.World journal of gastrointestinal surgery · 2025Article
- Integrated spatial omics of metabolic reprogramming and the tumor microenvironment in pancreatic cancer.iScience · 2025Article
- Innate Immunity and Platelets: Unveiling Their Role in Chronic Pancreatitis and Pancreatic Cancer.Cancers · 2025Review
- Radiomics reveals the biological basis for non-small cell lung cancer prognostic stratification by reflecting tumor immune microenvironment heterogeneity.Frontiers in immunology · 2025Article
- STAT5: Understanding the Biology of KRASJournal of cellular and molecular medicine · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy because it is often diagnosed at a late-stage. Signal transducer and activator of transcription 5 (STAT5) is a transcription factor implicated in the progression of various cancer types. However, its role in KRAS-driven pancreatic tumourigenesis remains unclear.
designWe performed studies with
resultsThe expression and phosphorylation of STAT5 were higher in human PDAC samples than control samples and high levels of STAT5 in tumour cells were associated with a poorer prognosis. The loss of STAT5 in pancreatic cells substantially reduces the KRAS mutation and pancreatitis-derived acinar-to-ductal metaplasia (ADM) and PDAC lesions. Mechanistically, we discovered that STAT5 binds directly to the promoters of ADM mediators, hepatocyte nuclear factor (HNF) 1β and HNF4α. Furthermore, STAT5 plays a crucial role in maintaining energy metabolism in tumour cells during PDAC progression. IL-22 signalling induced by chronic inflammation enhances KRAS-mutant-mediated STAT5 phosphorylation. Deficiency of IL-22 signalling slowed the progression of PDAC and ablated STAT5 activation.
conclusionCollectively, our findings identified pancreatic STAT5 activation as a key downstream effector of oncogenic KRAS signalling that is critical for ADM initiation and PDAC progression, highlighting its potential therapeutic vulnerability.
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