ArticleScientific reports2018
Inactivation of NUPR1 promotes cell death by coupling ER-stress responses with necrosis.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 72 citations in OpenAlex.
- Nuclear protein 1 is a cell death regulator in primary human airway epithelial cells and reduced in idiopathic pulmonary fibrosis.Scientific reports · 2026Article
- NUPR1 as a central stress-adaptation node in cancer: integrating metabolic rewiring, cell death, and therapy resistance.Journal of biomedical science · 2026Review
- An RNA-sequencing analysis to determine potential upstream transcriptional regulators of essential amino acid deficiency responses in bovine mammary epithelial cells.BMC genomics · 2026Article
- CDX2 confers ferroptosis resistance in stage II-III colon cancer via upregulation of NUPR1.Cell death & disease · 2026Article
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- Single cell transcriptomic analysis reveals pathogenic cell heterogeneity and candidate inflammatory-associated markers in STZ-induced diabetic mouse retina.Frontiers in immunology · 2026Article
- "Age is associated with Achilles tendon thickness in older adults: an ultrasound case-control study with intra-observer reliability".Frontiers in physiology · 2026Article
- A molecular circuit regulates fate plasticity in emerging and adult AT2 cells.Nature communications · 2025Article
- Development of an efficient NUPR1 inhibitor with anticancer activity.Scientific reports · 2024Article
- Current Technologies Unraveling the Significance of Post-Translational Modifications (PTMs) as Crucial Players in Neurodegeneration.Biomolecules · 2024Review
- Microgravity triggers ferroptosis and accelerates senescence in the MG-63 cell model of osteoblastic cells.NPJ microgravity · 2023Article
- [Mechanism of nuclear protein 1 in the resistance to axitinib in clear cell renal cell carcinoma].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
- Genome, Metabolism, or Immunity: Which Is the Primary Decider of Pancreatic Cancer Fate through Non-Apoptotic Cell Death?Biomedicines · 2023Review
- Tomatidine targets ATF4-dependent signaling and induces ferroptosis to limit pancreatic cancer progression.iScience · 2023Article
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- NUPR1 contributes to radiation resistance by maintaining ROS homeostasis via AhR/CYP signal axis in hepatocellular carcinoma.BMC medicine · 2022Article
- NUPR1 protects against hyperPARylation-dependent cell death.Communications biology · 2022Article
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- Transcriptional analysis of gasoline engine exhaust particulate matter 2.5-exposed human umbilical vein endothelial cells reveals the different gene expression patterns related to the cardiovascular diseases.Biochemistry and biophysics reports · 2022Article
- Characterization of the COPD alveolar niche using single-cell RNA sequencing.Nature communications · 2022Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
It was already described that genetic inhibition of NUPR1 induces tumor growth arrest. In this paper we studied the metabolism changes after NUPR1 downregulation in pancreatic cancer cells, which results in a significant decrease of OXPHOS activity with a concomitant lower ATP production which precedes the necrotic cell death. We demonstrated that NUPR1 downregulation induces a mitochondrial failure with a loss of the mitochondrial membrane potential, a strong increase in ROS production and a concomitant relocalization of mitochondria to the vicinity of the endoplasmic reticulum (ER). In addition, the transcriptomic analysis of NUPR1-deficient cells shows a decrease in the expression of some ER stress response-associated genes. Indeed, in ER stressors-treated cells with thapsigargin, brefeldin A or tunicamycin, a greater increase in necrosis and decrease of ATP content was observed in NUPR1-defficent cells. Finally, in vivo experiments, using acute pancreatitis which induces ER stress as well as NUPR1 activation, we observed that NUPR1 expression protects acinar cells from necrosis in mice. Importantly, we also report that the cell death observed after knocking-down NUPR1 expression is completely reversed by incubation with Necrostatin-1, but not by inhibiting caspase activity with Z-VAD-FMK. Altogether, these data enable us to describe a model in which inactivation of NUPR1 in pancreatic cancer cells results in an ER stress that induces a mitochondrial malfunction, a deficient ATP production and, as consequence, the cell death mediated by a programmed necrosis.
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