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The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells

ABSTRACT: The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells

PROVIDER: PRJNA483781 | ENA |

REPOSITORIES: ENA

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The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (Adherent MCF7 cells)

Project description:Since the thyroid hormone receptor β (TRβ) appears to suppress breast tumor growth and metastasis, we have analyzed the possibility that this receptor could affect cancer stem cell biology using TRβ-expressing MCF-7 cells (MCF7-TRβ cells) treated with the thyroid hormone T3.

2019-12-05 | GSE117949 | GEO

The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (mammospheres from MCF7 cells)

Project description:Since the thyroid hormone receptor β (TRβ) appears to suppress breast tumor growth and metastasis, we have analyzed the possibility that this receptor could affect cancer stem cell biology using mammospheres from TRβ-expressing MCF-7 cells (MCF7-TRβ cells) treated with the thyroid hormone T3.

2019-12-05 | GSE117950 | GEO

The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (Adherent MCF7 cells)

Project description:The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (Adherent MCF7 cells)

| PRJNA483784 | ENA

The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (mammospheres from MCF7 cells)

Project description:The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (mammospheres from MCF7 cells)

| PRJNA483782 | ENA

Thyroid Hormone Receptor ? Inhibits Self-Renewal Capacity of Breast Cancer Stem Cells.

Project description:Background: A subpopulation of cancer stem cells (CSCs) with capacity for self-renewal is believed to drive initiation, progression, and relapse of breast tumors. Methods: Since the thyroid hormone receptor ? (TR?) appears to suppress breast tumor growth and metastasis, we have analyzed the possibility that TR? could affect the CSC population using MCF-7 cells grown under adherent conditions or as mammospheres, as well as inoculation into immunodeficient mice. Results: Treatment of TR?-expressing MCF-7 cells (MCF7-TR? cells) with the thyroid hormone triiodothyronine (T3) decreased significantly CD44+/CD24- and ALDH+ cell subpopulations, the efficiency of mammosphere formation, the self-renewal capacity of CSCs in limiting dilution assays, the expression of the pluripotency factors in the mammospheres, and tumor initiating capacity in immunodeficient mice, indicating that the hormone reduces the CSC population present within the bulk MCF7-TR? cultures. T3 also decreased migration and invasion, a hallmark of CSCs. Transcriptome analysis showed downregulation of the estrogen receptor alpha (ER?) and ER-responsive genes by T3. Furthermore, among the T3-repressed genes, there was an enrichment in genes containing binding sites for transcription factors that are key determinants of luminal-type breast cancers and are required for ER binding to chromatin. Conclusion: We demonstrate a novel role of TR? in the biology of CSCs that may be related to its action as a tumor suppressor in breast cancer.

| S-EPMC6998057 | biostudies-literature

Next Generation Sequencing to assess pesticides capacity in vitro to act as agonists/antagonists of the thyroid hormone nuclear receptors

Project description:We combined in vitro tests to fully assess the capacity of pesticides to act as thyroid hormone disruptors (THD). Pesticides which were active in these tests were selected for a transcriptome analysis of neural cells. We took advantage of this technique to decipher what were the transcriptomic effects of these chemical in vitro. We also compared the expression of thyroid hormone responsive genes in presence or absence of the pesticides to determine if the transcriptomic changes could impact thyroid hormone receptor signaling. Although some pesticides elicit a cellular response, which sometimes interferes with thyroid hormone signaling, we found no evidence that they can act as TRα1 agonists or antagonists. We conclude that their neurodevelopmental toxicity in mammals is not explained by an alteration of the neural cell response to thyroid hormone.

2021-03-30 | GSE171038 | GEO

Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered an important site for thyroid action, the contribution of thyroid hormone receptor signaling, in muscle, to whole-body energy metabolism and body temperature has not been resolved. Here, we show that thyroid hormone-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRa1) in skeletal muscle, but that thyroid hormone induced elevation in body temperature is independent of muscle-TRa1. In slow-twitch soleus muscle, ablation of TRa1 leads to an altered fiber type composition toward a more oxidative phenotype, which, however, does not influence running capacity or motivation to voluntary running. RNA-sequencing of soleus muscle from WT mice and TRaHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, thus providing molecular clues pertaining to the mechanistic underpinnings of TRa1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in thyroid hormone-stimulated increase in whole-body energy expenditure.

2020-09-21 | GSE146336 | GEO

The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-05 | GSE117951 | GEO

Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

| PRJNA703005 | ENA

Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

Project description:Using tadpoles mutant for thyroid hormone receptor alpha (thra), we show that TRa is required for thyroid hormone (T3) induction of cell proliferation in the brain. RNA-sequencing showed that the TRa is required for 95% of the gene regulation responses to T3.

2019-05-13 | GSE130816 | GEO

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