ArticleOncogene2011
Mutation of thyroid hormone receptor-β in mice predisposes to the development of mammary tumors.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Review
- Clinical characteristics and survival of breast cancer patients with extramammary malignancies in a single Asian center over the past 23 years.Discover oncology · 2025Article
- Thyroid Hormone Receptors as Tumor Suppressors in Cancer.Endocrinology · 2024Review
- Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.International journal of molecular sciences · 2024Review
- Article
- Triiodothyronine lowers the potential of colorectal cancer stem cellsOncology reports · 2023Article
- Hormonal Crosstalk Between Thyroid and Breast Cancer.Endocrinology · 2022Review
- Article
- Prostate gland as a target organ of thyroid hormones: advances and controversies.Endocrine connections · 2022Review
- The TSH/Thyroid Hormones Axis and Breast Cancer.Journal of clinical medicine · 2022Review
- Thyroid hormones act as modulators of inflammation through their nuclear receptors.Frontiers in endocrinology · 2022Review
- Thyroid Hormone Receptor Beta as Tumor Suppressor: Untapped Potential in Treatment and Diagnostics in Solid Tumors.Cancers · 2021Review
- Targeting transcriptional regulators for treatment of anaplastic thyroid cancer.Journal of cancer metastasis and treatment · 2021Article
- Thyroid Hormone Receptor β Inhibits Self-Renewal Capacity of Breast Cancer Stem Cells.Thyroid : official journal of the American Thyroid Association · 2020Article
- Molecular Functions of Thyroid Hormone Signaling in Regulation of Cancer Progression and Anti-Apoptosis.International journal of molecular sciences · 2019Review
- Molecular functions and clinical impact of thyroid hormone-triggered autophagy in liver-related diseases.Journal of biomedical science · 2019Review
- 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
- Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor β.Molecular carcinogenesis · 2017Article
- Thyroid Hormone Controls Breast Cancer Cell Movement via Integrin αV/β3/SRC/FAK/PI3-Kinases.Hormones & cancer · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Correlative data suggest that thyroid hormone receptor-β (TRβ) mutations could increase the risk of mammary tumor development, but unequivocal evidence is still lacking. To explore the role of TRβ mutants in vivo in breast tumor development and progression, we took advantage of a knock-in mouse model harboring a mutation in the Thrb gene encoding TRβ (Thrb(PV) mouse). Although in adult nulliparous females, a single ThrbPV allele did not contribute to mammary gland abnormalities, the presence of two ThrbPV alleles led to mammary hyperplasia in ∼36% Thrb(PV/PV) mice. The ThrbPV mutation further markedly augmented the risk of mammary hyperplasia in a mouse model with high susceptibility to mammary tumors (Pten(+/-) mouse), as demonstrated by the occurrence of mammary hyperplasia in ∼60% of Thrb(PV/+)Pten(+/-) and ∼77% of Thrb(PV/PV)Pten(+/-) mice versus ∼33% of Thrb(+/+)Pten(+/-) mice. The Thrb(PV) mutation increased the activity of signal transducer and activator of transcription (STAT5) to increase cell proliferation and the expression of the STAT5 target gene encoding β-casein in the mammary gland. We next sought to understand the molecular mechanism underlying STAT5 overactivation by TRβPV. Cell-based studies with a breast cancer cell line (T47D cells) showed that thyroid hormone (T3) repressed STAT5 signaling in TRβ-expressing cells through decreasing STAT5-mediated transcription activity and target gene expression, whereas sustained STAT5 signaling was observed in TRβPV-expressing cells. Collectively, these findings show for the first time that a TRβ mutation promotes the development of mammary hyperplasia via aberrant activation of STAT5, thereby conferring a fertile genetic ground for tumorigenesis.
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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.