ArticleThe Journal of biological chemistry2013
Tumor-derived mutations in the gene associated with retinoid interferon-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3) activity and promote oncogenesis.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- The Mysterious Multitude: Structural Perspective on the Accessory Subunits of Respiratory Complex I.Frontiers in molecular biosciences · 2021Review
- Electron leak from NDUFA13 within mitochondrial complex I attenuates ischemia-reperfusion injury via dimerized STAT3.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The roles of signal transducer and activator of transcription factor 3 in tumor angiogenesis.Oncotarget · 2017Review
- GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.Cytokine & growth factor reviews · 2017Review
- STAT3 Undergoes Acetylation-dependent Mitochondrial Translocation to Regulate Pyruvate Metabolism.Scientific reports · 2016Article
- Mitochondrial GRIM-19 as a potential therapeutic target for STAT3-dependent carcinogenesis of gastric cancer.Oncotarget · 2016Article
- Disarming an Electrophilic Warhead: Retaining Potency in Tyrosine Kinase Inhibitor (TKI)-Resistant CML Lines While Circumventing Pharmacokinetic Liabilities.ChemMedChem · 2016Article
- High Glucose Induces Down-Regulated GRIM-19 Expression to Activate STAT3 Signaling and Promote Cell Proliferation in Cell Culture.PloS one · 2016Article
- Genomic and Transcriptomic Alterations Associated with STAT3 Activation in Head and Neck Cancer.PloS one · 2016Article
- Granulin, a novel STAT3-interacting protein, enhances STAT3 transcriptional function and correlates with poorer prognosis in breast cancer.Genes & cancer · 2015Article
- Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia.Leukemia · 2015Article
- Interferons, signal transduction pathways, and the central nervous system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Frequent mutation of receptor protein tyrosine phosphatases provides a mechanism for STAT3 hyperactivation in head and neck cancer.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Critical analysis of the potential for targeting STAT3 in human malignancy.OncoTargets and therapy · 2013Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The signal transducer and activator of transcription 3 (STAT3) protein is critical for multiple cytokine and growth factor-induced biological responses in vivo. Its transcriptional activity is controlled by a transient phosphorylation of a critical tyrosine. Constitutive activation of STAT3 imparts resistance to apoptosis, promotes cell proliferation, and induces de novo micro-angiogenesis, three of the six cardinal hallmarks of a typical cancer cell. Earlier we reported the isolation of GRIM-19 as a growth suppressor using a genome-wide expression knockdown strategy. GRIM-19 binds to STAT3 and suppresses its transcriptional activity. To understand the pathological relevance of GRIM-19, we screened a set of primary head and neck tumors and identified three somatic mutations in GRIM-19. Wild-type GRIM-19 suppressed cellular transformation by a constitutively active form of STAT3, whereas tumor-derived mutants L71P, L91P and A95T significantly lost their ability to associate with STAT3, block gene expression, and suppress cellular transformation and tumor growth in vivo. Additionally, these mutants lost their capacity to prevent metastasis. These mutations define a mechanism by which STAT3 activity is deregulated in certain human head and neck tumors.
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