ArticleOncogene2003
A novel mechanism of tumor suppression by destabilizing AU-rich growth factor mRNA.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 109 citations in OpenAlex.
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- Formation of Non-Nucleoplasmic Proteasome Foci during the Late Stage of Hyperosmotic Stress.Cells · 2021Article
- Tristetraprolin, a Potential Safeguard Against Carcinoma: Role in the Tumor Microenvironment.Frontiers in oncology · 2021Review
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- The Tristetraprolin Family of RNA-Binding Proteins in Cancer: Progress and Future Prospects.Cancers · 2020Review
- Identification of an AP1-ZFP36 Regulatory Network Associated with Breast Cancer Prognosis.Journal of mammary gland biology and neoplasia · 2020Article
- Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease.Frontiers in immunology · 2019Review
- Disease of mRNA Regulation: Relevance for Ischemic Brain Injury.Translational stroke research · 2018Review
- Cell cycle RNA regulons coordinating early lymphocyte development.Wiley interdisciplinary reviews. RNA · 2017Review
- Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017Review
- Nuclear tristetraprolin acts as a corepressor of multiple steroid nuclear receptors in breast cancer cells.Molecular genetics and metabolism reports · 2016Article
- Computational Reconstruction of NFκB Pathway Interaction Mechanisms during Prostate Cancer.PLoS computational biology · 2016Article
- Evolution and Biological Roles of Alternative 3'UTRs.Trends in cell biology · 2016Review
- Three Residues Make an Evolutionary Switch for Folding and RNA-Destabilizing Activity in the TTP Family of Proteins.ACS chemical biology · 2016Article
- RNA binding proteins as regulators of immune cell biology.Clinical and experimental immunology · 2016Review
- Stress granules, P-bodies and cancer.Biochimica et biophysica acta · 2015Review
- ZFP36 stabilizes RIP1 via degradation of XIAP and cIAP2 thereby promoting ripoptosome assembly.BMC cancer · 2015Article
- Tristetraprolin inhibits the growth of human glioma cells through downregulation of urokinase plasminogen activator/urokinase plasminogen activator receptor mRNAs.Molecules and cells · 2015Article
- RNase L attenuates mitogen-stimulated gene expression via transcriptional and post-transcriptional mechanisms to limit the proliferative response.The Journal of biological chemistry · 2014Article
- Transforming growth factor β regulates P-body formation through induction of the mRNA decay factor tristetraprolin.Molecular and cellular biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The occurrence of pathologically stable mRNAs of proto-oncogenes, growth factors and cyclins has been proposed to contribute to experimental and human oncogenesis. In normal resting cells, mRNAs containing an AU-rich element (ARE) in their 3' untranslated region are subjected to rapid degradation. Tristetraprolin (TTP) is an RNA-binding zinc-finger protein that promotes decay of ARE-containing mRNAs. Here we report that TTP acts as a potent tumor suppressor in a v-H-ras-dependent mast cell tumor model, where tumors express abnormally stable interleukin-3 (IL-3) mRNA as part of an oncogenic autocrine loop. Premalignant v-H-ras cells were transfected with TTP and injected into syngeneic mice. TTP expression delayed tumor progression by 4 weeks, and late appearing tumors escaped suppression by loss of TTP. When transfected into a fully established tumor line, TTP reduced cloning efficiency in vitro and growth of the inoculated cells in vivo. Transgenic TTP interfered with the autocrine loop by enhancing the degradation of IL-3 mRNA with concomitant reduction of IL-3 secretion. Our data establish the ARE as an antioncogenic target in a model situation, underline the importance of mRNA stabilization in oncogenesis and show for the first time that tumor suppression can be achieved by interfering with mRNA turnover.
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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.