ArticleJournal of neuro-oncology2013
Mutant tristetraprolin: a potent inhibitor of malignant glioma cell growth.
Article in Journal of neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
- Inhibition of the RNA Regulator HuR by SRI-42127 Attenuates Neuropathic Pain After Nerve Injury Through Suppression of Neuroinflammatory Responses.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- The versatile role of HuR in Glioblastoma and its potential as a therapeutic target for a multi-pronged attack.Advanced drug delivery reviews · 2022Review
- Cottonseed-derived gossypol and ethanol extracts differentially regulate cell viability and VEGF gene expression in mouse macrophages.Scientific reports · 2021Article
- Kinome inhibition reveals a role for polo-like kinase 1 in targeting post-transcriptional control in cancer.Molecular oncology · 2021Article
- Tristetraprolin, Inflammation, and Metabolic Syndrome in Arab Adults: A Case Control Study.Biology · 2021Article
- Protein phosphatase 2A as a therapeutic target in inflammation and neurodegeneration.Pharmacology & therapeutics · 2019Review
- [Tristetraprolin inhibits autophagy in cultured lung cancer cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Roles of Tristetraprolin in Tumorigenesis.International journal of molecular sciences · 2018Review
- Post-transcriptional regulation of cytokine and growth factor signaling in cancer.Cytokine & growth factor reviews · 2017Review
- Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017Review
- The control of inflammation via the phosphorylation and dephosphorylation of tristetraprolin: a tale of two phosphatases.Biochemical Society transactions · 2016Review
- The RNA-binding protein TTP is a global post-transcriptional regulator of feedback control in inflammation.Nucleic acids research · 2016Article
- Inactivation of tristetraprolin in chronic hypoxia provokes the expression of cathepsin B.Molecular and cellular biology · 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
- Hu antigen R (HuR) is a positive regulator of the RNA-binding proteins TDP-43 and FUS/TLS: implications for amyotrophic lateral sclerosis.The Journal of biological chemistry · 2014Article
- Steering tumor progression through the transcriptional response to growth factors and stroma.FEBS letters · 2014Review
- Identification of a major phosphopeptide in human tristetraprolin by phosphopeptide mapping and mass spectrometry.PloS one · 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
11 authors at 3 institutions in 1 country.
Funding
Abstract
Malignant gliomas rely on the production of certain critical growth factors including VEGF, interleukin (IL)-6 and IL-8, to fuel rapid tumor growth, angiogenesis, and treatment resistance. Post-transcriptional regulation through adenine and uridine-rich elements of the 3' untranslated region is one mechanism for upregulating these and other growth factors. In glioma cells, we have shown that the post-transcriptional machinery is optimized for growth factor upregulation secondary to overexpression of the mRNA stabilizer, HuR. The negative regulator, tristetraprolin (TTP), on the other hand, may be suppressed because of extensive phosphorylation. Here we test that possibility by analyzing the phenotypic effects of a mutated form of TTP (mt-TTP) in which 8 phosphoserine residues were converted to alanines. We observed a significantly enhanced negative effect on growth factor expression in glioma cells at the post-transcriptional and transcriptional levels. The protein became stabilized and displayed significantly increased antiproliferative effects compared to wild-type TTP. Macroautophagy was induced with both forms of TTP, but inhibition of autophagy did not affect cell viability. We conclude that glioma cells suppress TTP function through phosphorylation of critical serine residues which in turn contributes to growth factor upregulation and tumor progression.
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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.