ArticleOncotarget2015
Oncogenic mutations of thyroid hormone receptor β.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.International journal of molecular sciences · 2024Review
- TRβ Agonism Induces Tumor Suppression and Enhances Drug Efficacy in Anaplastic Thyroid Cancer in Female Mice.Endocrinology · 2023Article
- Common tumor-suppressive signaling of thyroid hormone receptor beta in breast and thyroid cancer cells.Molecular carcinogenesis · 2021Article
- Thyroid Hormone Receptor Beta Inhibits PI3K-Akt-mTOR Signaling Axis in Anaplastic Thyroid Cancer via Genomic Mechanisms.Journal of the Endocrine Society · 2021Article
- Thyroid Hormone Receptor Beta Induces a Tumor-Suppressive Program in Anaplastic Thyroid Cancer.Molecular cancer research : MCR · 2020Article
- Inherited Genetic Mutations and Polymorphisms in Malignant Mesothelioma: A Comprehensive Review.International journal of molecular sciences · 2020Review
- Sonic Hedgehog and Triiodothyronine Pathway Interact in Mouse Embryonic Neural Stem Cells.International journal of molecular sciences · 2020Article
- The Thyroid Hormone Receptor-RUNX2 Axis: A Novel Tumor Suppressive Pathway in Breast Cancer.Hormones & cancer · 2020Article
- Higher order genomic organization and epigenetic control maintain cellular identity and prevent breast cancer.Genes, chromosomes & cancer · 2019Review
- Overexpression of modified human TRβ1 suppresses the growth of hepatocarcinoma SK-hep1 cells in vitro and in xenograft models.Molecular and cellular biochemistry · 2018Article
- Review of the possible association between thyroid and breast carcinoma.World journal of surgical oncology · 2018Review
- Overexpressing modified human TRβ1 suppresses the proliferation of breast cancer MDA-MB-468 cells.Oncology letters · 2018Article
- Analysis of Thyroid Tumorigenesis in Xenograft Mouse Model.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Crosstalk between integrin αvβ3 and ERα contributes to thyroid hormone-induced proliferation of ovarian cancer cells.Oncotarget · 2017Article
- Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor β.Molecular carcinogenesis · 2017Article
- Relationship between the expression of TRβ1 and the molecular typing and clinicopathological features of breast cancer.International journal of clinical and experimental pathology · 2017Article
- Inhibition of STAT3 signaling blocks obesity-induced mammary hyperplasia in a mouse model.American journal of cancer research · 2017Article
- ChIP-on-chip analysis of thyroid hormone-regulated genes and their physiological significance.Oncotarget · 2016Article
- Thyroid hormone and anti-apoptosis in tumor cells.Oncotarget · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The C-terminal frame-shift mutant of the thyroid hormone receptor TRβ1, PV, functions as an oncogene. An important question is whether the oncogenic activity of mutated TRβ1 is uniquely dependent on the PV mutated sequence. Using four C-terminal frame-shift mutants-PV, Mkar, Mdbs, and AM-we examined that region in the oncogenic actions of TRβ1 mutants. Remarkably, these C-terminal mutants induced similar growth of tumors in mouse xenograft models. Molecular analyses showed that they physically interacted with the p85α regulatory subunit of PI3K similarly in cells. In vitro GST-binding assay showed that they bound to the C-terminal Src-homology 2 (CSH2) of p85α with markedly higher avidity. The sustained association of mutants with p85α led to activation of the common PI3K-AKT-ERK/STAT3 signaling to promote cell proliferation and invasion and to inhibit apoptosis. Thus, these results argue against the oncogenic activity of PV being uniquely dependent on the PV mutated sequence. Rather, these four mutants could favor a C-terminal conformation that interacted with the CSH2 domain of p85α to initiate activation of PI3K to relay downstream signaling to promote tumorigenesis. Thus, we propose that the mutated C-terminal region of TRβ1 could function as an "onco-domain" and TRβ1 is a potential therapeutic target.
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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.