ArticleMolecular cancer research : MCR2012
The mRNA stability factor HuR inhibits microRNA-16 targeting of COX-2.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 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
111 citing papers in PubMed, 207 citations in OpenAlex.
- ELAVL1 Promotes Proliferation and Inhibits Apoptosis of the Marek's Disease Virus (MDV)-Transformed Cell Line MSB1 via the COX-2/PGE2 Pathway.Animals : an open access journal from MDPI · 2026Article
- The multifaceted role of microRNAs in colorectal cancer: pathogenesis and therapeutic implications.Non-coding RNA research · 2025Review
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies.Frontiers in immunology · 2025Review
- Unraveling the Regulatory Role of HuR/microRNA Axis in Colorectal Cancer Tumorigenesis.Cancers · 2024Review
- A spatiotemporally resolved atlas of mRNA decay in thebioRxiv : the preprint server for biology · 2024Article
- CBS-HJournal of advanced research · 2023Article
- MicroRNAs miR-16 and miR-519 control meningioma cell proliferationFrontiers in oncology · 2023Article
- MicroRNAs, Tristetraprolin Family Members and HuR: A Complex Interplay Controlling Cancer-Related Processes.Cancers · 2022Review
- AGO-RBP crosstalk on target mRNAs: Implications in miRNA-guided gene silencing and cancer.Translational oncology · 2022Review
- HuR-dependent SOD2 protein synthesis is an early adaptation to anchorage-independence.Redox biology · 2022Article
- Cell-Penetrating Peptide TAT-HuR-HNS3 Suppresses Proinflammatory Gene Expression via Competitively Blocking Interaction of HuR with Its Partners.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Factors influencing degradation kinetics of mRNAs and half-lives of microRNAs, circRNAs, lncRNAs in blood in vitro using quantitative PCR.Scientific reports · 2022Article
- Review
- Review
- The versatile role of HuR in Glioblastoma and its potential as a therapeutic target for a multi-pronged attack.Advanced drug delivery reviews · 2022Review
- Modulation of miRISC-Mediated Gene Silencing in Eukaryotes.Frontiers in molecular biosciences · 2022Review
- PACER lncRNA regulates COX-2 expression in lung cancer cells.Oncotarget · 2022Article
- Drug delivery approaches for HuR-targeted therapy for lung cancer.Advanced drug delivery reviews · 2022Review
- Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Exploration of the Hsa-miR-1587-Protein Interaction and the Inhibition to CASK.International journal of molecular sciences · 2021Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Commonly observed in colorectal cancer is the elevated expression of the prostaglandin (PG) synthase COX-2. In normal intestinal epithelium, the COX-2 mRNA is targeted for rapid decay through the 3'-untranslated region (3'-UTR) adenylate- and uridylate (AU)-rich element (ARE), whereas in tumors ARE-mediated decay is compromised. Here we show that the COX-2 ARE can mediate degradation through microRNA (miRNA)-mediated regulation. We identified miR-16 to bind the COX-2 3'-UTR and inhibit COX-2 expression by promoting rapid mRNA decay. In colorectal cancer cells and tumors, miR-16 levels were decreased approximately twofold and miR-16 expression in cancer cells attenuated COX-2 expression and PG synthesis. The COX-2 ARE is also bound by the RNA-binding protein HuR. In colorectal cancer tumors, HuR is overexpressed and localized within the cytoplasm, where it promotes ARE-mRNA stabilization. Under conditions of HuR overexpression, miR-16 was unable to promote rapid mRNA decay through the COX-2 ARE. Ribonucleoprotein immunoprecipitation of HuR showed direct association with miR-16 that was reversed when cytoplasmic trafficking of HuR was inhibited. Furthermore, this interaction between HuR and miR-16 promoted the downregulation of miR-16. These new results identify miR-16 as a central posttranscriptional regulator of COX-2 and show the ability of elevated levels of HuR to antagonize miR-16 function. Along with insight into altered ARE-mediated mRNA decay observed in colorectal cancer, these findings provide a new explanation for tumor-derived loss of miR-16.
Indexed as
Identifiers
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.