ArticleCancer research2015
IL17 Functions through the Novel REG3β-JAK2-STAT3 Inflammatory Pathway to Promote the Transition from Chronic Pancreatitis to Pancreatic Cancer.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- An axon-intrinsic loop restricts nerve regeneration through axonal protein synthesis.Science advances · 2026Article
- GATA4 loss promotes mutantbioRxiv : the preprint server for biology · 2026Article
- Unveiling the gut-pancreas axis: microbial influence on stemness and tumor microenvironment of PDAC.Stem cells (Dayton, Ohio) · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Aging modulation of the immune system and immunotherapy efficacy in cancer.Frontiers in immunology · 2026Review
- REG3A: A Multifunctional Antioxidant Lectin at the Crossroads of Microbiota Regulation, Inflammation, and Cancer.Cancers · 2025Review
- REG3A secreted by peritumoral acinar cells enhances pancreatic ductal adenocarcinoma progression via activation of EGFR signaling.Cell communication and signaling : CCS · 2025Article
- A sex dependent association between the history of autoimmune disease and the development of pancreatic cancer: a case-control study of 32,640 patients.Frontiers in oncology · 2025Article
- Correlation Between Antihypertensive Drugs and Survival Among Patients with Pancreatic Ductal Adenocarcinoma.Cancers · 2024Review
- Macrophages and T cells in metabolic disorder-associated cancers.Nature reviews. Cancer · 2024Review
- Role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer (Review).Oncology reports · 2024Review
- Pancreatic stellate cells and the interleukin family: Linking fibrosis and immunity to pancreatic ductal adenocarcinoma (Review).Molecular medicine reports · 2024Review
- Current and future immunotherapeutic approaches in pancreatic cancer treatment.Journal of hematology & oncology · 2024Review
- Gut epithelial Interleukin-17 receptor A signaling can modulate distant tumors growth through microbial regulation.Cancer cell · 2024Article
- Role of STAT3 in pancreatic cancer.Exploration of targeted anti-tumor therapy · 2024Review
- The role of interleukin-17 in inflammation-related cancers.Frontiers in immunology · 2024Review
- Increased circulating Th17 cell populations in patients with pancreatic ductal adenocarcinoma.Immunogenetics · 2023Article
- Mechanistic Insights into the Roles of the IL-17/IL-17R Families in Pancreatic Cancer.International journal of molecular sciences · 2023Review
- IL-17A-producing CD8Gut · 2023Article
8 more citing papers are in PubMed but not listed here.
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13 authors at 6 institutions in 4 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) offers an optimal model for discovering "druggable" molecular pathways that participate in inflammation-associated cancer development. Chronic pancreatitis, a common prolonged inflammatory disease, behaves as a well-known premalignant condition that contributes to PDAC development. Although the mechanisms underlying the pancreatitis-to-cancer transition remain to be fully elucidated, emerging evidence supports the hypothesis that the actions of proinflammatory mediators on cells harboring Kras mutations promote neoplastic transformation. Recent elegant studies demonstrated that the IL17 pathway mediates this phenomenon and can be targeted with antibodies, but the downstream mechanisms by which IL17 functions during this transition are currently unclear. In this study, we demonstrate that IL17 induces the expression of REG3β, a well-known mediator of pancreatitis, during acinar-to-ductal metaplasia and in early pancreatic intraepithelial neoplasia (PanIN) lesions. Furthermore, we found that REG3β promotes cell growth and decreases sensitivity to cell death through activation of the gp130-JAK2-STAT3-dependent pathway. Genetic inactivation of REG3β in the context of oncogenic Kras-driven PDAC resulted in reduced PanIN formation, an effect that could be rescued by administration of exogenous REG3β. Taken together, our findings provide mechanistic insight into the pathways underlying inflammation-associated pancreatic cancer, revealing a dual and contextual pathophysiologic role for REG3β during pancreatitis and PDAC initiation.
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