ArticleOncogene2009
Thyroid hormone receptor mutants implicated in human hepatocellular carcinoma display an altered target gene repertoire.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Transforming Cancer Diagnostics: The Emergence of Liquid Biopsy and Epigenetic Markers.MedComm · 2025Review
- Actions of thyroid hormones and thyromimetics on the liver.Nature reviews. Gastroenterology & hepatology · 2025Review
- Protective effect of higher free thyroxine levels within the reference range on biliary tract cancer risk: a multivariable mendelian randomization and mediation analysis.Frontiers in endocrinology · 2024Article
- Thyroid Hormone in Hepatocellular Carcinoma: Cancer Risk, Growth Regulation, and Anticancer Drug Resistance.Frontiers in medicine · 2020Review
- Thyroid hormones concentration in portal and peripheral blood in patients with pancreatic cancer: Preliminary study.Cancer biomarkers : section A of Disease markers · 2020Observational
- Mislocalization of Cancer-associated Thyroid Hormone Receptor Mutants.Nuclear receptor research · 2020Article
- Thyroid Hormones and Cancer: A Comprehensive Review of Preclinical and Clinical Studies.Frontiers in endocrinology · 2019Review
- The Role of Thyroid Hormones in Hepatocyte Proliferation and Liver Cancer.Frontiers in endocrinology · 2019Review
- Thyroid hormone suppresses hepatocarcinogenesis via DAPK2 and SQSTM1-dependent selective autophagy.Autophagy · 2016Article
- Chemotherapy resistance and metastasis-promoting effects of thyroid hormone in hepatocarcinoma cells are mediated by suppression of FoxO1 and Bim pathway.Cell death & disease · 2016Article
- Hepatocellular carcinoma: thyroid hormone promotes tumorigenicity through inducing cancer stem-like cell self-renewal.Scientific reports · 2016Article
- Autoregulatory loop of nuclear corepressor 1 expression controls invasion, tumor growth, and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The functional significance of common polymorphisms in zinc finger transcription factors.G3 (Bethesda, Md.) · 2014Article
- microRNAs 424 and 503 are mediators of the anti-proliferative and anti-invasive action of the thyroid hormone receptor beta.Oncotarget · 2014Article
- The role of thyroid hormone signaling in the prevention of digestive system cancers.International journal of molecular sciences · 2013Review
- Thyroid hormone actions in liver cancer.Cellular and molecular life sciences : CMLS · 2013Review
- Molecular functions of thyroid hormones and their clinical significance in liver-related diseases.BioMed research international · 2013Review
- Thyroid hormone receptors promote metastasis of human hepatoma cells via regulation of TRAIL.Cell death and differentiation · 2012Article
- Stable isotope labeling with amino acids in cell culture (SILAC)-based quantitative proteomics study of a thyroid hormone-regulated secretome in human hepatoma cells.Molecular & cellular proteomics : MCP · 2012Article
- Genetic features of thyroid hormone receptors.Journal of genetics · 2012Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that control multiple aspects of normal physiology and development. Mutations in TRs have been identified at high frequency in certain cancers, including human hepatocellular carcinomas (HCCs). The majority of HCC-TR mutants bear lesions within their DNA recognition domains, and we have hypothesized that these lesions change the mutant receptors' target gene repertoire in a way crucial to their function as oncoproteins. Using stable cell transformants and expression array analysis, we determined that mutant TRs isolated from two different HCCs do, as hypothesized, display a target gene repertoire distinct from that of their normal TR progenitors. Only a subset of genes regulated by wild-type TRs was regulated by the corresponding HCC-TR mutants. More surprisingly, the HCC-TR mutants also gained the ability to regulate additional target genes not recognized by the wild-type receptors, and were not simply restricted to repression, but could also activate a subset of their target genes. We conclude that the TR mutants isolated from HCC have sustained multiple alterations from their normal progenitors that include not only changes in their transcriptional outputs, but also changes in the genes they target; both are likely to contribute to neoplasia.
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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.