ArticlePloS one2011
MiR-224 targets the 3'UTR of type 1 5'-iodothyronine deiodinase possibly contributing to tissue hypothyroidism in renal cancer.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- MicroRNAs in renal cell carcinoma: a systematic review of clinical implications (Review).Oncology reports · 2015Pooled it
- Evaluating the performance of multi-omics integration: a thyroid toxicity case study.Archives of toxicology · 2025Article
- Diagnostic, prognostic, and therapeutic potential of exosomal microRNAs in renal cancer.Pharmacological reports : PR · 2024Review
- TAZ upregulates MIR-224 to inhibit oxidative stress response in multiple myeloma.Cancer reports (Hoboken, N.J.) · 2023Article
- Histone deacetylase 3 promotes alveolar epithelial-mesenchymal transition and fibroblast migration under hypoxic conditions.Experimental & molecular medicine · 2022Article
- A Concise Review of MicroRNA-383: Exploring the Insights of Its Function in Tumorigenesis.Journal of Cancer · 2022Review
- mRNA-miRNA networks identify metabolic pathways associated to the anti-tumorigenic effect of thyroid hormone on preneoplastic nodules and hepatocellular carcinoma.Frontiers in oncology · 2022Article
- Deiodinases and Cancer.Endocrinology · 2021Review
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- Paradigms of Dynamic Control of Thyroid Hormone Signaling.Endocrine reviews · 2019Review
- miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Article
- Cardiac Thyroid Hormone Metabolism and Heart Failure.European thyroid journal · 2017Review
- Upregulated microRNA-224 promotes ovarian cancer cell proliferation by targeting KLLN.In vitro cellular & developmental biology. Animal · 2017Article
- Article
- Clinical value and potential targets of miR-224-5p in hepatocellular carcinoma validated by a TCGA- and GEO- based study.International journal of clinical and experimental pathology · 2017Article
- Aberrantly expressed microRNAs in bladder cancer and renal cell carcinoma.Journal of human genetics · 2017Review
- miR-224-3p inhibits autophagy in cervical cancer cells by targeting FIP200.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 iodothyronine deiodinase (DIO1) catalyses the conversion of prohormone thyroxine to the active thyroid hormone 3,3',5-triiodothyronine (T3), important regulator of cell proliferation and differentiation. DIO1 expression is reduced in the most common type of kidney neoplasia, clear cell Renal Cell Carcinoma (ccRCC). MicroRNAs are small, non-coding RNAs that regulate gene expression at posttranscriptional levels. The aim of this study was to analyze the potential regulation of DIO1 expression by microRNAs in ccRCC. Bioinformatic analysis revealed that 3'UTR of the human DIO1 gene transcript contains miR-224 and miR-383 target sites, which are conserved across mammalian species. Semi-quantitative real-time PCR was used to analyze the expression of miR-224 and miR-383 in 32 samples of ccRCC tumors (T) and in 32 matched control (C) samples. We observed statistically significant (p = 0.0002) more than four fold increase in miR-224 expression and nearly two fold increase in miR-383 expression in samples T compared to samples C. Tumor specific changes in expression of miR-224 negatively correlated with changes in DIO1 expression and intracellular T3 concentration. Transfection of HeLa cell line with miR-224 and miR-383 suppressed the activity of a luciferase reporter containing the 3'UTR of DIO1. This was abolished when constructs mutated at the miR-224 and miR-383 target sites were used instead, indicating that miR-224 and miR-383 directly bind to DIO1 3'UTR. Finally, induced expression of miR-224 in Caki-2 cells resulted in significant (p<0.01) reduction of DIO1 mRNA. This study provides a novel miRNA-mediated regulatory mechanism of DIO1 expression in ccRCC.
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