ReviewAgeing research reviews2012
Tristetraprolin: roles in cancer and senescence.
Review in Ageing research reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 61 citations in OpenAlex.
- Functional interplay between TTP/ZFP36 and HuR/ELAVL1 in cancer: a post-transcriptional regulatory network.Frontiers in oncology · 2026Review
- Cytoplasmic regulation of the poly(A) tail length as a potential therapeutic target.RNA (New York, N.Y.) · 2025Review
- SMARCD1 is an essential expression-restricted metastasis modifier.Communications biology · 2024Article
- Necrosis score as a prognostic factor in stage I-III colorectal cancer: a retrospective multicenter study.Discover oncology · 2023Article
- Tristetraprolin regulates phagocytosis through interaction with CD47 in head and neck cancer.Experimental and therapeutic medicine · 2022Article
- Advances in the study of RNA-binding proteins in diabetic complications.Molecular metabolism · 2022Review
- Targeting Zinc Finger Proteins with Exogenous Metals and Molecules: Lessons learned from Tristetraprolin, a CCCH type Zinc Finger.European journal of inorganic chemistry · 2021Article
- Targeting Tristetraprolin Expression or Functional Activity Regulates Inflammatory Response Induced by MSU Crystals.Frontiers in immunology · 2021Article
- Tumor suppressing effects of tristetraprolin and its small double-stranded RNAs in bladder cancer.Cancer medicine · 2021Article
- GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- The Senescence-Associated Secretory Phenotype (SASP) in the Challenging Future of Cancer Therapy and Age-Related Diseases.Biology · 2020Review
- Wnt/CTNNB1 Signal Transduction Pathway Inhibits the Expression of ZFP36 in Squamous Cell Carcinoma, by Inducing Transcriptional Repressors SNAI1, SLUG and TWIST.International journal of molecular sciences · 2020Article
- Identification of an AP1-ZFP36 Regulatory Network Associated with Breast Cancer Prognosis.Journal of mammary gland biology and neoplasia · 2020Article
- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Promoter Methylation Leads to DecreasedFrontiers in medicine · 2020Article
- Protein phosphatase 2A as a therapeutic target in inflammation and neurodegeneration.Pharmacology & therapeutics · 2019Review
- The tandem zinc finger RNA binding domain of members of the tristetraprolin protein family.Wiley interdisciplinary reviews. RNA · 2019Review
- Translating the Hypoxic Response-the Role of HIF Protein Translation in the Cellular Response to Low Oxygen.Cells · 2019Review
- Dysregulation of tristetraprolin and human antigen R promotes gastric cancer progressions partly by upregulation of the high-mobility group box 1.Scientific reports · 2018Article
- The ARE-binding protein Tristetraprolin (TTP) is a novel target and mediator of calcineurin tumor suppressing function in the skin.PLoS genetics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer and senescence are both complex transformative processes that dramatically alter many features of cell physiology and their interactions with surrounding tissues. Developing the wide range of cellular features characteristic of these conditions requires profound alterations in global gene expression patterns, which can be achieved by suppressing, activating, or uncoupling cellular gene regulatory pathways. Many genes associated with the initiation and development of tumors are regulated at the level of mRNA decay, frequently through the activity of AU-rich mRNA-destabilizing elements (AREs) located in their 3'-untranslated regions. As such, cellular factors that recognize and control the decay of ARE-containing mRNAs can influence tumorigenic or senescent phenotypes mediated by products of these transcripts. In this review, we discuss evidence showing how suppressed expression and/or activity of the ARE-binding protein tristetraprolin (TTP) can contribute to these processes. Next, we outline current findings linking TTP suppression to exacerbation of individual tumorigenic phenotypes, and the roles of specific TTP substrate mRNAs in mediating these effects. Finally, we survey potential mechanisms that cells may employ to suppress TTP expression in cancer, and propose potential diagnostic and therapeutic strategies that may exploit the relationship between TTP expression and tumor progression or senescence.
Indexed as
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What OpenQuestion holds
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.