ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2009
Down-regulation of GRIM-19 expression is associated with hyperactivation of STAT3-induced gene expression and tumor growth in human cervical cancers.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Low Expression of GRIM-19 Correlates with Poor Prognosis in Patients with Upper Urinary Tract Urothelial Carcinoma.Current cancer drug targets · 2025Article
- GRIM-19 deficiency promotes clear cell renal cell carcinoma progression and is associated with high TNM stage and Fuhrman grade.Oncology letters · 2020Article
- Article
- TheGenes · 2018Review
- Article
- GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.Cytokine & growth factor reviews · 2017Review
- A natural food sweetener with anti-pancreatic cancer properties.Oncogenesis · 2016Article
- STAT3:FOXM1 and MCT1 drive uterine cervix carcinoma fitness to a lactate-rich microenvironment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- GRIM-19 mutations fail to inhibit v-Src-induced oncogenesis.Oncogene · 2014Article
- Overexpression of GRIM-19, a mitochondrial respiratory chain complex I protein, suppresses hepatocellular carcinoma growth.International journal of clinical and experimental pathology · 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
- 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.The Journal of biological chemistry · 2013Article
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- Downregulation of GRIM-19 is associated with hyperactivation of p-STAT3 in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2012Article
- GRIM-19 disrupts E6/E6AP complex to rescue p53 and induce apoptosis in cervical cancers.PloS one · 2011Article
- GRIM-19 and p16(INK4a) synergistically regulate cell cycle progression and E2F1-responsive gene expression.The Journal of biological chemistry · 2010Article
- Review
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Cervical cancer is the most common malignant disease responsible for the deaths of a large number of women in the developing world. Although certain strains of human papillomavirus (HPV) have been identified as the cause of this disease, events that lead to formation of malignant tumors are not fully clear. STAT3 is a major oncogenic transcription factor involved in the development and progression of a number of human tumors. However, the mechanisms that result in loss of control over STAT3 activity are not understood. Gene associated with Retinoid-Interferon-induced Mortality-19 (GRIM-19) is a tumor-suppressive protein identified using a genetic technique in the interferon/retinoid-induced cell death pathway. Here, we show that reduction in GRIM-19 protein levels occur in a number of primary human cervical cancers. Consequently, these tumors tend to express a high basal level of STAT3 and its downstream target genes. More importantly, using a surrogate model, we show that restoration of GRIM-19 levels reestablishes the control over STAT3-dependent gene expression and tumor growth in vivo. GRIM-19 suppressed the expression of tumor invasion- and angiogenesis-associated factors to limit tumor growth. This study identifies another major novel molecular pathway inactivated during the development of human cervical cancer.
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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.