ArticleOncogene2006
Restoration of SHIP-1 activity in human leukemic cells modifies NF-kappaB activation pathway and cellular survival upon oxidative stress.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 61 citations in OpenAlex.
- SLAM-family receptors promote resolution of ILC2-mediated inflammation.Nature communications · 2024Article
- Dauricine Protects from LPS-Induced Bone Loss via the ROS/PP2A/NF-κB Axis in Osteoclasts.Antioxidants (Basel, Switzerland) · 2020Article
- Oxidative stress and inflammation in a spectrum of epileptogenic cortical malformations: molecular insights into their interdependence.Brain pathology (Zurich, Switzerland) · 2019Article
- Hydrogen Peroxide Triggers a Dual Signaling Axis To Selectively Suppress Activated Human T Lymphocyte Migration.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- IKKα regulates human keratinocyte migration through surveillance of the redox environment.Journal of cell science · 2017Article
- IKKβ promotes metabolic adaptation to glutamine deprivation via phosphorylation and inhibition of PFKFB3.Genes & development · 2016Article
- Redox homeostasis: The Golden Mean of healthy living.Redox biology · 2016Article
- Detrimental role of pericyte Nox4 in the acute phase of brain ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies.Cancer metastasis reviews · 2015Review
- Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways.Frontiers in microbiology · 2015Article
- Macrophage mitochondrial oxidative stress promotes atherosclerosis and nuclear factor-κB-mediated inflammation in macrophages.Circulation research · 2014Article
- Role of inositol poly-phosphatases and their targets in T cell biology.Frontiers in immunology · 2013Review
- IKK-β mediates hydrogen peroxide induced cell death through p85 S6K1.Cell death and differentiation · 2013Article
- Erythrocytes induce proinflammatory endothelial activation in hypoxia.American journal of respiratory cell and molecular biology · 2013Article
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- The bad, the good, and the ugly about oxidative stress.Oxidative medicine and cellular longevity · 2012Review
- TPEN induces apoptosis independently of zinc chelator activity in a model of acute lymphoblastic leukemia and ex vivo acute leukemia cells through oxidative stress and mitochondria caspase-3- and AIF-dependent pathways.Oxidative medicine and cellular longevity · 2012Article
- Basic principles and emerging concepts in the redox control of transcription factors.Antioxidants & redox signaling · 2011Review
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- Article
Corrections and comments
- Expression of concern
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor-kappa B (NF-kappaB) is an important prosurvival transcription factor activated in response to a large array of external stimuli, including reactive oxygen species (ROS). Previous works have shown that NF-kappaB activation by ROS involved tyrosine phosphorylation of the inhibitor IkappaBalpha through an IkappaB kinase (IKK)-independent mechanism. In the present work, we investigated with more details NF-kappaB redox regulation in human leukemic cells. By using different cell lines (CEM, Jurkat and the subclone Jurkat JR), we clearly showed that NF-kappaB activation by hydrogen peroxide (H2O2) is cell-type dependent: it activates NF-kappaB through tyrosine phosphorylation of IkappaBalpha in Jurkat cells, whereas it induces an IKK-mediated IkappaBalpha phosphorylation on S32 and 36 in CEM and Jurkat JR cells. We showed that this H2O2-induced IKK activation in CEM and Jurkat JR cells is mediated by SH2-containing inositol 5'-phosphatase 1 (SHIP-1), a lipid phosphatase that is absent in Jurkat cells. Indeed, the complementation of SHIP-1 in Jurkat cells made them shift to an IKK-dependent mechanism upon oxidative stress stimulation. We also showed that Jurkat cells expressing SHIP-1 are more resistant to H2O2-induced apoptosis than the parental cells, suggesting that SHIP-1 has an important role in leukemic cell responses to ROS in terms of signal transduction pathways and apoptosis resistance, which can be of interest in improving ROS-mediated chemotherapies.
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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.