ArticleThe Journal of clinical investigation2012
Myeloid cell expression of the RNA-binding protein HuR protects mice from pathologic inflammation and colorectal carcinogenesis.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 127 citations in OpenAlex.
- Loss of Pum2 exacerbates colitis by disrupting macrophage-epithelial crosstalk and promoting epithelial necroptosis.Cell death discovery · 2026Article
- HuR Knockdown in MLO-Y4 Osteocyte-like Cells Elevates OPG Expression and Suppresses Osteoclastogenesis In Vitro.International journal of molecular sciences · 2025Article
- DENetwork unveils non-differentially expressed genes with functional relevance across conditions through information flow perturbation.Nucleic acids research · 2025Article
- Article
- Integrated pan-cancer analysis of RNA binding protein HuR investigates its biomarker potential in prognosis, immunotherapy, and drug sensitivity.PLoS computational biology · 2025Article
- HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Role of Tumor-Intrinsic HuR in Modeling the Pancreatic Tumor Microenvironment: Molecular Mechanisms and Therapeutic Opportunities.Molecular and cellular biology · 2025Review
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies.Frontiers in immunology · 2025Review
- Novel, soluble 3-heteroaryl-substituted tanshinone mimics attenuate the inflammatory response in murine macrophages.Scientific reports · 2024Article
- Review
- CircDCBLD2 alleviates liver fibrosis by regulating ferroptosis via facilitating STUB1-mediated PARK7 ubiquitination degradation.Journal of gastroenterology · 2024Article
- RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024Review
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- NK cell expansion requires HuR and mediates control of solid tumors and long-term virus infection.The Journal of experimental medicine · 2023Article
- Relationship between HuR and tumor drug resistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- HuR modulation counteracts lipopolysaccharide response in murine macrophages.Disease models & mechanisms · 2023Article
- Eltrombopag Inhibits Metastasis in Breast Carcinoma by Targeting HuR Protein.International journal of molecular sciences · 2023Article
- The poly(C)-binding protein Pcbp2 is essential for CD4iScience · 2023Article
- RNA as a Major-Groove Ligand: RNA-RNA and RNA-DNA Triplexes Formed by GAA and UUC or TTC Sequences.ACS omega · 2022Article
- HuR as a molecular target for cancer therapeutics and immune-related disorders.Advanced drug delivery reviews · 2022Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The innate immune response involves a variety of inflammatory reactions that can result in inflammatory disease and cancer if they are not resolved and instead are allowed to persist. The effective activation and resolution of innate immune responses relies on the production and posttranscriptional regulation of mRNAs encoding inflammatory effector proteins. The RNA-binding protein HuR binds to and regulates such mRNAs, but its exact role in inflammation remains unclear. Here we show that HuR maintains inflammatory homeostasis by controlling macrophage plasticity and migration. Mice lacking HuR in myeloid-lineage cells, which include many of the cells of the innate immune system, displayed enhanced sensitivity to endotoxemia, rapid progression of chemical-induced colitis, and severe susceptibility to colitis-associated cancer. The myeloid cell-specific HuR-deficient mice had an exacerbated inflammatory cytokine profile and showed enhanced CCR2-mediated macrophage chemotaxis. At the molecular level, activated macrophages from these mice showed enhancements in the use of inflammatory mRNAs (including Tnf, Tgfb, Il10, Ccr2, and Ccl2) due to a lack of inhibitory effects on their inducible translation and/or stability. Conversely, myeloid overexpression of HuR induced posttranscriptional silencing, reduced inflammatory profiles, and protected mice from colitis and cancer. Our results highlight the role of HuR as a homeostatic coordinator of mRNAs that encode molecules that guide innate inflammatory effects and demonstrate the potential of harnessing the effects of HuR for clinical benefit against pathologic inflammation and 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.