ArticleOncogene2008
Thyroid hormone receptor-beta (TR beta 1) impairs cell proliferation by the transcriptional inhibition of cyclins D1, E and A2.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed.
- Thyroid receptor β might be responsible for breast cancer associated with Hashimoto's thyroiditis: a new insight into pathogenesis.Immunologic research · 2022Review
- Ezh2 promotes TRβ lysine methylation-mediated degradation in hepatocellular carcinoma.Genes & genomics · 2022Article
- Article
- Selective Inhibition of Genomic and Non-Genomic Effects of Thyroid Hormone Regulates Muscle Cell Differentiation and Metabolic Behavior.International journal of molecular sciences · 2021Article
- Thyroid Hormone Receptor Beta Induces a Tumor-Suppressive Program in Anaplastic Thyroid Cancer.Molecular cancer research : MCR · 2020Article
- Thyroid Hormones as Renal Cell Cancer Regulators.Journal of signal transduction · 2016Review
- Role of cyclins in controlling progression of mammalian spermatogenesis.The International journal of developmental biology · 2013Review
- SRY-box containing gene 17 regulates the Wnt/β-catenin signaling pathway in oligodendrocyte progenitor cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- The thyroid hormone receptors as modulators of skin proliferation and inflammation.The Journal of biological chemistry · 2011Article
- Thyroid hormone - triiodothyronine - has contrary effect on proliferation of human proximal tubules cell line (HK2) and renal cancer cell lines (Caki-2, Caki-1) - role of E2F4, E2F5 and p107, p130.Thyroid research · 2008Article
- Involvement of cyclins in mammalian spermatogenesis.Molecular and cellular biochemistry · 2008Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormone receptor-beta1 (TRbeta1) belongs to the ligand-inducible transcription factor superfamily. We have previously described that stable TRbeta1 expression impairs fibroblast proliferation diminishing levels and activity of the main regulators of the G(1)/S transition. To unmask the underlying molecular mechanism of this action, we have investigated the expression of cyclin D1, E and A2 upon serum stimulation in TRbeta1 expressing cells, finding a strong downregulation of their mRNAs, concomitant with low protein levels. The inhibition of the transcriptional activation in response to serum of these cyclins is differently exerted. For cyclin D1, we demonstrate that TRbeta1 represses its promoter as a consequence of the downregulation of c-jun levels, diminished AP-1 activation and loss of c-jun recruitment to its binding sites on cyclin D1 promoter. For cyclin E and A2, it is the impairment of the cyclinD/Rb/E2F pathway by TRbeta1 that prevents the activation of these two E2F target genes. Indeed, recruitment of E2F-1 to cyclin A2 promoter could not be detected. In summary, we propose that apo-TRbeta1 exerts its antiproliferative action through a mechanism that could constitute a model by which other nuclear receptors may control cell division.
Indexed as
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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.