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Thyroid Hormone Receptor Beta Induces a Tumor Suppressive Program in Anaplastic Thyroid Cancer

ABSTRACT: Thyroid Hormone Receptor Beta Induces a Tumor Suppressive Program in Anaplastic Thyroid Cancer

PROVIDER: PRJNA631915 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11776776.fastq.gz	Fastqsanger.gz
	SRR11776777.fastq.gz	Fastqsanger.gz
	SRR11776778.fastq.gz	Fastqsanger.gz
	SRR11776779.fastq.gz	Fastqsanger.gz
	SRR11776780.fastq.gz	Fastqsanger.gz

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Similar Datasets

Thyroid Hormone Receptor Beta Induces a Tumor Suppressive Program in Anaplastic Thyroid Cancer

Project description:The thyroid hormone receptor beta (TRβ), a key regulator of cellular growth and differentiation, is frequently dysregulated in cancers. Diminished expression of TRb is noted in thyroid, breast, and other solid tumors and is correlated with more aggressive disease. Restoration of TRb levels decreased tumor growth supporting the concept that TRb could function as a tumor suppressor. Yet, the TRb tumor suppression transcriptome is not well delineated and the impact of TRb is unknown in aggressive anaplastic thyroid cancer (ATC). Here, we establish that restoration of TRb expression in the human ATC cell line SW1736 (SW-TRβ) reduces the aggressive phenotype, decreases cancer stem-cell populations and induces cell death in a T3-dependent manner. Transcriptomic analysis of SW-TRβ cells via RNA-sequencing revealed distinctive expression patterns induced by ligand-bound TRβ and revealed novel molecular signaling pathways. Of note, liganded TRβ repressed multiple nodes in the PI3K/AKT pathway, induced expression of thyroid differentiation markers, and promoted pro-apoptotic pathways. Our results further revealed the JAK1-STAT1 pathway as a novel, T3-mediated, anti-tumorigenic pathway that can be activated in additional ATC lines. These findings elucidate a TRb-driven tumor suppression transcriptomic signature, highlight unexplored therapeutic options for ATC, and support TRb activation as a promising therapeutic option in cancers.

2020-05-13 | GSE150364 | GEO

Common Tumor Suppressive Signaling of Thyroid Hormone Receptor Beta in Breast and Thyroid Cancer Cells

Project description:The thyroid hormone receptor beta (TRβ) is a tumor suppressor in multiple types of solid tumors, most prominently in breast and thyroid cancer. An increased understanding of the molecular mechanisms by which TRβ abrogates tumorigenesis could aid in understanding the core tumor suppressive program that TRβ facilitates. Here, we introduce TRβ into the MDA-MB-468 basal-like breast cancer cell line and perform RNA-sequencing to determine changes in transcriptomic signaling. The TRβ expressing MDA-MB-468 cells exhibit a more epithelial character as determined by PCA-PAM50 score and through repression of mesenchymal cytokeratins. The epithelial to mesenchymal transition pathway is also significantly reduced. The MDA-MB-468 dataset was also compared to RNA sequencing results from the thyroid cancer line SW1736 to determine which genes are TRβ regulated across both tissue types. Stearate biosynthesis was revealed as upregulated from the shared gene set, a lipid which is known to repress breast tumorigenesis, as were chromatin remodeling pathways. These data provide novel insights into the molecular mechanisms by which TRβ suppresses breast tumorigenesis and suggests a common metabolic role in breast and thyroid cancer as well a role for TRβ in the maintenance of epithelial cellular identity.

2021-09-21 | GSE151479 | GEO

PIAS2b dsRNAi repression kills by mitotic catastrophe anaplastic thyroid and non-thyroid carcinomas, but not normal thyroid or differentiated carcinomas

Project description:The E3 SUMO ligase PIAS2 is expressed at high levels in differentiated papillary thyroid carcinomas but at low levels in anaplastic thyroid carcinomas (ATC), an undifferentiated cancer with very high mortality. Double-stranded RNA–directed RNA interference (dsRNAi) targeting the PIAS2 isoform beta (PIAS2b) inhibits growth of ATC cell lines and patient primary cultures in vitro and orthotopic patient-derived xenografts (oPDX) in vivo, but not of thyroid cell lines or non-anaplastic primary thyroid cultures (differentiated carcinoma, benign lesions, or normal). PIAS2b-dsRNAi also has an anti-cancer effect on other anaplastic human cancers (pancreas, lung, and gastric). Mechanistically, PIAS2b is required for proper mitotic spindle and centrosome assembly, and it is a dosage-sensitive protein in ATC. Strikingly, PIAS2b-dsRNAi induces mitotic catastrophe at prophase. High-throughput proteomics revealed the proteasome (PSMC5) and spindle cytoskeleton as direct targets of PIAS2b SUMOylation at mitotic initiation. PIAS2b-dsRNAi is a promising therapy for ATC and other aggressive anaplastic cancers.

2024-04-08 | PXD044110 | Pride

Thyroid Hormone Receptor Beta Induces a Tumor-Suppressive Program in Anaplastic Thyroid Cancer.

Project description:The thyroid hormone receptor beta (TRβ), a key regulator of cellular growth and differentiation, is frequently dysregulated in cancers. Diminished expression of TRβ is noted in thyroid, breast, and other solid tumors and is correlated with more aggressive disease. Restoration of TRβ levels decreased tumor growth supporting the concept that TRβ could function as a tumor suppressor. Yet, the TRβ tumor suppression transcriptome is not well delineated and the impact of TRβ is unknown in aggressive anaplastic thyroid cancer (ATC). Here, we establish that restoration of TRβ expression in the human ATC cell line SW1736 (SW-TRβ) reduces the aggressive phenotype, decreases cancer stem cell populations and induces cell death in a T3-dependent manner. Transcriptomic analysis of SW-TRβ cells via RNA sequencing revealed distinctive expression patterns induced by ligand-bound TRβ and revealed novel molecular signaling pathways. Of note, liganded TRβ repressed multiple nodes in the PI3K/AKT pathway, induced expression of thyroid differentiation markers, and promoted proapoptotic pathways. Our results further revealed the JAK1-STAT1 pathway as a novel, T3-mediated, antitumorigenic pathway that can be activated in additional ATC lines. These findings elucidate a TRβ-driven tumor suppression transcriptomic signature, highlight unexplored therapeutic options for ATC, and support TRβ activation as a promising therapeutic option in cancers. IMPLICATIONS: TRβ-T3 induced a less aggressive phenotype and tumor suppression program in anaplastic thyroid cancer cells revealing new potential therapeutic targets.

| S-EPMC7541631 | biostudies-literature

Normal thyrocytes vs papillary vs anaplastic thyroid carcinomas

Project description:We profiled the gene expression of 11 anaplastic thyroid carcinomas (ATC), 49 papillary thyroid carcinomas (PTC) and 45 normal thyroids (N) We hibridized a series of anaplastic thyroid carcinomas (ATC) and papillary thyroid carcinomas (PTC) onto Affymetrix U133 Plus 2.0 arrays. ATCs were obtained from different hospitals in France and Belgium. Paired RNA samples of PTCs and non-tumoral thyroid tissues were obtained from Ukraine via the Chernobyl Tissue Bank (www.chernobyltissuebank.com). Diagnoses were confirmed by the members of the International Pathology Panel of the Chernobyl Tissue Bank.

2012-11-09 | E-GEOD-33630 | biostudies-arrayexpress

Normal thyrocytes vs papillary vs anaplastic thyroid carcinomas

Project description:We profiled the gene expression of 11 anaplastic thyroid carcinomas (ATC), 49 papillary thyroid carcinomas (PTC) and 45 normal thyroids (N)

2012-11-09 | GSE33630 | GEO

Common Tumor Suppressive Signaling of Thyroid Hormone Receptor Beta in Breast and Thyroid Cancer Cells

Project description:Common Tumor Suppressive Signaling of Thyroid Hormone Receptor Beta in Breast and Thyroid Cancer Cells

| PRJNA635931 | ENA

RNA-seq of anaplastic thyroid carcinoma cells (CAL62 and 8505c) after E2F7 silencing

Project description:Gene expression comparison between anaplastic thyroid carcinoma cells (CAL62 and 8505c) transfected with si-RNA against E2F7 or scramble oligos, with the intent of defining the gene expression program under the control of this transcription factor in this tumor subtype.

2023-02-07 | E-MTAB-9788 | biostudies-arrayexpress

RNA-seq of anaplastic thyroid carcinoma cell line (8505c) after overexpression of OVOL2

Project description:Identification of OVOL2-related transcriptional program in anaplastic thyroid carcinoma-derived cell line, 8505c. Doxycycline-inducible system was obtained by infecting 8505c cells with lentiviral vector containing OVOL2 coding sequence fused with HA tag. Control cells were infected with empty vector (EV). Cells were collected 24 hours upon doxycycline treatment.

2023-10-05 | E-MTAB-11055 | biostudies-arrayexpress

Sporadic vs. Post-Chernobyl Papillary vs. Anaplastic Thyroid Cancers

Project description:We profiled the gene expression of anaplastic thyroid cancers of Belgian patients. We compared these with the expression profile of a cohort of papillary thyroid tumors both from the Chernobyl Tissues Bank (CTB) and French patients with no history of exposure to radiations, along with their patient-matched healthy adjacent thyroid.

2012-06-01 | GSE29265 | GEO

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