ArticleOncogene2012
Consequences of DJ-1 upregulation following p53 loss and cell transformation.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Protein deglycase DJ-1 deficiency aggravates acute viral myocarditis by promoting apoptosis via reducing Dusp1 expression.Cell death & disease · 2025Article
- Article
- The Imbalance of p53-Park7 Signaling Axis Induces Iron Homeostasis Dysfunction in Doxorubicin-Challenged Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- PARK7/DJ-1 as a Therapeutic Target in Gut-Brain Axis Diseases.International journal of molecular sciences · 2022Review
- Biomarkers in the diagnosis of pancreatic cancer: Are we closer to finding the golden ticket?World journal of gastroenterology · 2021Review
- Cytoprotective Mechanisms of DJ-1: Implications in Cardiac Pathophysiology.Molecules (Basel, Switzerland) · 2021Review
- Parkinson's disease: Alterations in iron and redox biology as a key to unlock therapeutic strategies.Redox biology · 2021Review
- Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis.Progress in retinal and eye research · 2021Review
- DJ‑1 is a new prognostic marker and predicts chemotherapy efficacy in colorectal cancer.Oncology reports · 2020Article
- DJ-1 promotes epithelial-to-mesenchymal transition via enhancing FGF9 expression in colorectal cancer.Biology open · 2020Article
- Novel Insights into PARK7 (DJ-1), a Potential Anti-Cancer Therapeutic Target, and Implications for Cancer Progression.Journal of clinical medicine · 2020Review
- DJ-1 promotes colorectal cancer progression through activating PLAGL2/Wnt/BMP4 axis.Cell death & disease · 2018Article
- Cytoprotective mechanisms of DJ-1 against oxidative stress through modulating ERK1/2 and ASK1 signal transduction.Redox biology · 2018Review
- Metabolic Reprogramming and the Recovery of Physiological Functionality in 3D Cultures in Micro-Bioreactors.Bioengineering (Basel, Switzerland) · 2018Article
- Park 7: A Novel Therapeutic Target for Macrophages in Sepsis-Induced Immunosuppression.Frontiers in immunology · 2018Review
- Regulation of Signal Transduction by DJ-1.Advances in experimental medicine and biology · 2017Article
- Subcellular localization of DJ-1 in human HL-60 leukemia cells in response to diallyl disulfide treatment.Molecular medicine reports · 2016Article
- DJ-1 Is Upregulated in Oral Squamous Cell Carcinoma and Promotes Oral Cancer Cell Proliferation and Invasion.Journal of Cancer · 2016Article
- Deficiency of DJ-1 Ameliorates Liver Fibrosis through Inhibition of Hepatic ROS Production and Inflammation.International journal of biological sciences · 2016Article
- Chronic Inflammation Links Cancer and Parkinson's Disease.Frontiers in aging neuroscience · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 is a tumor suppressor that responds to various stress signals by initiating cell-cycle arrest, senescence and apoptosis. Mutations of the p53 gene are found in over 50% of human tumors, highlighting the importance of p53 in tumor suppression. Numerous studies have reported on the interactions between p53, IGF-1-AKT and mTOR pathways as potentially explaining some of the tumor suppressive activities of p53. To further understand the basis of these interactions, we analyzed the involvement of DJ-1, an oncogene known to drive AKT-mediated cell survival, in the p53-AKT axis. In this study, we show that DJ-1 and p53 are tightly 'linked': p53 prevents the accumulation of DJ-1 protein, whereas loss of p53 leads to stabilization and enhancement of DJ-1 expression. Interestingly, this increase in DJ-1 level is only observed when p53 loss is accompanied by transformation of cells. Moreover, DJ-1 seems to be required for the enhanced activation of AKT observed in p53-deficient cells. Such observation confers a new property to DJ-1 associated to transforming-process to its oncogenic ability to drive AKT activation. We also show that DJ-1 is necessary for p53 activation following oxidative stress, suggesting the existence of a finely regulated loop between these two proteins in transformed cells. Finally, we demonstrate that in the absence of p53, DJ-1 is stabilized by ROS accumulation, and surprisingly seems to be required for this high intracellular ROS production. These data offer new insights into the regulation of DJ-1 and suggest that DJ-1 is a target of p53. Importantly, our study highlights that during transformation, DJ-1 is having a key role in the p53-regulated AKT pathway and p53-driven oxidative-stress response.
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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.