ArticleMolecular and cellular biology2004
The thyroid hormone receptor is a suppressor of ras-mediated transcription, proliferation, and transformation.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed.
- The key roles of thyroid hormone in mitochondrial regulation, at interface of human health and disease.Journal of basic and clinical physiology and pharmacology · 2024Review
- Triiodothyronine lowers the potential of colorectal cancer stem cellsOncology reports · 2023Article
- Regulation of metabolic and transcriptional responses by the thyroid hormone in cellular models of murine macrophages.Frontiers in immunology · 2022Article
- Thyroid hormones act as modulators of inflammation through their nuclear receptors.Frontiers in endocrinology · 2022Review
- Thyroid hormone receptor alpha sumoylation modulates white adipose tissue stores.Scientific reports · 2021Article
- Article
- Thyroid hormone receptor β sumoylation is required for thyrotropin regulation and thyroid hormone production.JCI insight · 2021Article
- Article
- Thyroid hormones in diabetes, cancer, and aging.Aging cell · 2020Review
- The Thyroid Hormone Receptor-RUNX2 Axis: A Novel Tumor Suppressive Pathway in Breast Cancer.Hormones & cancer · 2020Article
- Deiodinases and their intricate role in thyroid hormone homeostasis.Nature reviews. Endocrinology · 2019Review
- Neoepitope targets of tumour-infiltrating lymphocytes from patients with pancreatic cancer.British journal of cancer · 2019Article
- Thyroid Hormones and Cancer: A Comprehensive Review of Preclinical and Clinical Studies.Frontiers in endocrinology · 2019Review
- The Antiarrhythmic Drug, Dronedarone, Demonstrates Cytotoxic Effects in Breast Cancer Independent of Thyroid Hormone Receptor Alpha 1 (THRα1) Antagonism.Scientific reports · 2018Article
- Thyroid Hormone Receptor β Suppression of RUNX2 Is Mediated by Brahma-Related Gene 1-Dependent Chromatin Remodeling.Endocrinology · 2018Article
- Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor β.Molecular carcinogenesis · 2017Article
- Thyroid Hormone Receptor-β (TRβ) Mediates Runt-Related Transcription Factor 2 (Runx2) Expression in Thyroid Cancer Cells: A Novel Signaling Pathway in Thyroid Cancer.Endocrinology · 2016Article
- Oncogenic mutations of thyroid hormone receptor β.Oncotarget · 2015Article
- Mutation analysis underlying the downregulation of the thyroid hormone receptor β1 gene in the Chinese breast cancer population.OncoTargets and therapy · 2015Article
- Thyroid hormone increases bulk histones expression by enhancing translational efficiency.Molecular endocrinology (Baltimore, Md.) · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The thyroid hormone triiodothyronine (T3) has a profound effect on growth, differentiation, and metabolism in higher organisms. Here we demonstrate that T3 inhibits ras-induced proliferation in neuroblastoma cells and blocks induction of cyclin D1 expression by the oncogene. The hormone, at physiological concentrations, strongly antagonizes the transcriptional response mediated by the Ras/mitogen-activated protein kinase/ribosomal-S6 subunit kinase (Rsk) signaling pathway in cells expressing thyroid hormone receptors (TRs). T3 blocks the response to the oncogenic forms of the three ras isoforms (H-, K-, and N-ras) and both TRalpha and TRbeta can mediate this action. The main target for induction of cyclin D1 transcription by oncogenic ras in neuroblastoma cells is a cyclic AMP response element (CRE) located in proximal promoter sequences, and T3 represses the transcriptional activity of b-Zip transcription factors such as CREB (CRE-binding protein) or ATF-2 (activation transcription factor 2) that are direct targets of Rsk2 and bind to this sequence. The hormone also blocks fibroblast transformation by oncogenic ras when TR is expressed. Furthermore, TRs act as suppressors of tumor formation by the oncogene in vivo in nude mice. The TRbeta isoform has stronger antitransforming properties than the alpha isoform and can inhibit tumorigenesis even in hypothyroid mice. These results show the existence of a previously unrecognized transcriptional cross talk between the TRs and the ras oncogene which influences relevant processes such as cell proliferation, transformation, or tumorigenesis.
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.