ArticleMolecular endocrinology (Baltimore, Md.)2012
Identification of microRNAs that mediate thyroid cell growth induced by TSH.
Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Quantitative assessment of preoperative serum thyrotropin level and thyroid cancer.Oncotarget · 2016Pooled it
- Circulating microRNA expression underlying the association of opioid use with low bone mineral density.JBMR plus · 2026Article
- LncRNA LIPE-AS1 Predicts Poor Survival of Cervical Cancer and Promotes Its Proliferation and Migration via Modulating miR-195-5p/MAPK Pathway.Frontiers in oncology · 2021Article
- microRNA-339-5p modulates Na+/I- symporter-mediated radioiodide uptake.Endocrine-related cancer · 2015Article
- MicroRNA in teleost fish.Genome biology and evolution · 2014Review
- Thyroglobulin increases thyroid cell proliferation via the suppression of specific microRNAs.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Article
- MiRNA expression may account for chronic but not for acute regulation of mRNA expression in human thyroid tumor models.PloS one · 2014Article
- Multiplicity of hormone-secreting tumors: common themes about cause, expression, and management.The Journal of clinical endocrinology and metabolism · 2013Review
- Differential expression profiling and functional analysis of microRNAs through stage I-III papillary thyroid carcinoma.International journal of medical sciences · 2013Article
- MicroRNA expression array identifies novel diagnostic markers for conventional and oncocytic follicular thyroid carcinomas.The Journal of clinical endocrinology and metabolism · 2013Article
- Regulation of dual oxidase expression and H2O2 production by thyroglobulin.Thyroid : official journal of the American Thyroid Association · 2012Article
- Propylthiouracil increases sodium/iodide symporter gene expression and iodide uptake in rat thyroid cells in the absence of TSH.Thyroid : official journal of the American Thyroid Association · 2012Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TSH is a major regulator of thyroid cell growth and endocrine function. It is known that cAMP and phosphatidylinositol 3-kinase (PI3K) are responsible for mediating the action of TSH. Activation of these signals results in the induction of a series of transcription factors and cell cycle regulating proteins, which induce cell proliferation. In addition to such canonical transcriptional regulation, it was recently shown that microRNA (miRNA or miR) constitutes another key mechanism for the regulation of gene expression. However, whether TSH action is mediated by miRNA in the thyroid is unknown. In this study, we have performed miRNA microarray analysis and demonstrated that TSH significantly decreases expression of 47 miRNA in thyroid cells. Among these, we have shown, using their specific agonists, that overexpression of miR-16 and miR-195 suppressed cell cycle progression and DNA synthesis that was induced by TSH. In silico analysis predicted that Mapk8, Ccne1, and Cdc6, the expression of which was up-regulated by TSH, are potential target genes for these miRNA, and overexpression of miR-16 and miR-195 suppressed expression of these target genes. The decrease of miR-16 and miR-195 expression by TSH was reproduced by forskolin and N(6),2'-O-dibutyryladenosine cAMP and reversed by the protein kinase A inhibitor H89 and the PI3K inhibitor LY294002. These results suggest that TSH activates cAMP/protein kinase A and PI3K cascades to decrease miR-16 and miR-195, which induce Mapk8, Ccne1, and Cdc6 to activate cell proliferation.
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