ArticleThe Journal of clinical investigation2012
Nuclear protein 1 promotes pancreatic cancer development and protects cells from stress by inhibiting apoptosis.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 125 citations in OpenAlex.
- NF-κB inducing kinase (NIK) deletion accelerates KRAS-driven pancreatic cancer in association with tumor microenvironment remodeling.Cell death & disease · 2026Article
- GATA4 loss promotes mutantbioRxiv : the preprint server for biology · 2026Article
- NUPR1 as a central stress-adaptation node in cancer: integrating metabolic rewiring, cell death, and therapy resistance.Journal of biomedical science · 2026Review
- Article
- Dual molecular and clinical machine-learning prognostic modeling in pancreatic ductal adenocarcinoma: a chaperone-mediated autophagy-based framework integrating multi-cohort molecular signatures and a single-center clinical nomogram.Frontiers in cell and developmental biology · 2026Article
- Targeting intrinsically disordered nuclear protein 1 (NUPR1) with single-domain antibodies alleviates triple-negative breast cancer (TNBC) progression in vivo.Cell death & disease · 2025Article
- c-Rel drives pancreatic cancer metastasis through fibronectin-integrin signaling-induced isolation stress resistance and EMT.Molecular cancer · 2025Article
- Downregulation of the CCK-B Receptor in Pancreatic Stellate Cells Blocks Molecular Proliferative Pathways and Increases Apoptosis to Decrease Pancreatic Cancer Growth In Vitro.International journal of molecular sciences · 2025Article
- Self-assembling dendrimer nanodrug formulations for decreased hERG-related toxicity and enhanced therapeutic efficacy.Science advances · 2025Article
- Correlation study of NF-κB, IER3, and Recurrence of Ovarian Endometrioid Cysts.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- IER3: exploring its dual function as an oncogene and tumor suppressor.Cancer gene therapy · 2025Article
- NEMO/NF-κB signaling functions as a double-edged sword in PanIN formation versus progression to pancreatic cancer.Molecular cancer · 2024Article
- Elucidating the role of intrinsic adenosine A1 receptors in acute alcoholism using human-induced pluripotent stem cell-derived hepatocytes.Bioscience reports · 2024Article
- Targeting NUPR1-dependent stress granules formation to induce synthetic lethality in KrasEMBO molecular medicine · 2024Article
- Exploring Hypertrophic Cardiomyopathy Biomarkers through Integrated Bioinformatics Analysis: Uncovering Novel Diagnostic Candidates.Cardiology research and practice · 2024Article
- Microgravity triggers ferroptosis and accelerates senescence in the MG-63 cell model of osteoblastic cells.NPJ microgravity · 2023Article
- Cell-in-Cell Structures in Gastrointestinal Tumors: Biological Relevance and Clinical Applications.Journal of personalized medicine · 2023Review
- Review
- Review
- NUPR1 protects against hyperPARylation-dependent cell death.Communications biology · 2022Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) has the lowest survival rate of all cancers and shows remarkable resistance to cell stress. Nuclear protein 1 (Nupr1), which mediates stress response in the pancreas, is frequently upregulated in pancreatic cancer. Here, we report that Nupr1 plays an essential role in pancreatic tumorigenesis. In a mouse model of pancreatic cancer with constitutively expressed oncogenic Kras(G12D), we found that loss of Nupr1 protected from the development of pancreatic intraepithelial neoplasias (PanINs). Further, in cultured pancreatic cells, nutrient deprivation activated Nupr1 expression, which we found to be required for cell survival. We found that Nupr1 protected cells from stress-induced death by inhibiting apoptosis through a pathway dependent on transcription factor RelB and immediate early response 3 (IER3). NUPR1, RELB, and IER3 proteins were coexpressed in mouse PanINs from Kras(G12D)-expressing pancreas. Moreover, pancreas-specific deletion of Relb in a Kras(G12D) background resulted in delayed in PanIN development associated with a lack of IER3 expression. Thus, efficient PanIN formation was dependent on the expression of Nupr1 and Relb, with likely involvement of IER3. Finally, in patients with PDAC, expression of NUPR1, RELB, and IER3 was significantly correlated with a poor prognosis. Cumulatively, these results reveal a NUPR1/RELB/IER3 stress-related pathway that is required for oncogenic Kras(G12D)-dependent transformation of the pancreas.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.