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Global transcriptome analysis indicates that depletion of rps13 and ribosomes leads to cell cycle arrest in G1

ABSTRACT: Affymetrix Toxoplasma microarray data was analyzed to determine whether there was an association with a G1 transcript profile. Four hundred seventy-five genes with significant gene expression differences (Welch T-test, P = 0.01) between ±ATc samples were identified. Genes were clustered into those increased (153) or decreased (322) -ATc. There are a number of genes with diminished expression and pronounced over expression -ATc including LDH1, 4 zinc finger proteins, leucine-rich protein, and ABC transporter-like molecules, myosin-related molecules with many fold increases and one AP2 protein with a small increase. These gene sets have a large overlap with G1 genes defined in an ongoing cell cycle expression study in T. gondii (Behnke, White). Over 60% of those genes that have diminished expression -ATc overlap with genes that are diminished at G1, and over 40% of genes with increased expression -ATc overlap with genes that are up regulated at G1. A hypergeometric distribution of this association suggests that the probability of this happening by chance is essentially zero. Thus, by both methods, FACS and arrays, parasites -ATc display a G1 profile.

ORGANISM(S): Toxoplasma gondii

PROVIDER: GSE20616 | GEO | 2010/11/29

SECONDARY ACCESSION(S): PRJNA124799

REPOSITORIES: GEO

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Global transcriptome analysis indicates that depletion of rps13 and ribosomes leads to cell cycle arrest in G1

Project description:Affymetrix Toxoplasma microarray data was analyzed to determine whether there was an association with a G1 transcript profile. Four hundred seventy-five genes with significant gene expression differences (Welch T-test, P = 0.01) between ±ATc samples were identified. Genes were clustered into those increased (153) or decreased (322) -ATc. There are a number of genes with diminished expression and pronounced over expression -ATc including LDH1, 4 zinc finger proteins, leucine-rich protein, and ABC transporter-like molecules, myosin-related molecules with many fold increases and one AP2 protein with a small increase. These gene sets have a large overlap with G1 genes defined in an ongoing cell cycle expression study in T. gondii (Behnke, White). Over 60% of those genes that have diminished expression -ATc overlap with genes that are diminished at G1, and over 40% of genes with increased expression -ATc overlap with genes that are up regulated at G1. A hypergeometric distribution of this association suggests that the probability of this happening by chance is essentially zero. Thus, by both methods, FACS and arrays, parasites -ATc display a G1 profile. To determine the global transcriptional differences of the RSP13 conditional mutant with and without anhydrotetracycline (ATc). Four replicates each.

2010-11-29 | E-GEOD-20616 | biostudies-arrayexpress

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

Project description:Anaplastic thyroid carcinoma (ATC) is one of the most aggressive malignancy and accounts for the majority of thyroid cancer-related deaths. Despite intensive research, there remains no effective treatment for patients with ATC. Here, we identify THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7), as a potent anti-ATC compound by high-throughput chemical screening. ATC cells, but not papillary thyroid cancer (PTC) cells, are exceptionally sensitive to CDK7 inhibition. Analyzing both gene expression profiles and super enhancer (SE) features reveals that the SE-mediated oncogenic transcriptional amplification renders the vulnerability of ATC cells to THZ1 treatment. Combining this integrative analysis with functional assays discovers a number of novel cancer genes of ATC, including PPP1R15A, SMG9 and KLF2. Inhibition of PPP1R15A with Guanabenz (GBZ) or Sephin1 greatly suppresses ATC growth. Significantly, the expression level of PPP1R15A is correlated with CDK7 expression in ATC tissue samples. Elevated expression of PPP1R15A and CDK7 are both associated with poor clinical prognosis in ATC patients. Importantly, GBZ or THZ1 treatment sensitizes ATC cells to conventional chemotherapy. Taken together, these findings demonstrate transcriptional addiction in ATC pathobiology and identify CDK7 and PPP1R15A as potential biomarkers and therapeutic targets for ATC.

2019-03-01 | GSE120177 | GEO

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

2019-03-01 | GSE120176 | GEO

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [ChIP-Seq]

2019-03-01 | GSE120175 | GEO

Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma [RNA-seq]

Project description:Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer, with no effective treatment available. Identification of new anti-ATC drugs represents an urgent need. In this study, we find that ATC cells are highly sensitive to THZ531, a potent inhibitor of the transcriptional cyclin-dependent kinase (CDK), CDK12. Cell-based assays demonstrate that CDK12 inhibition significantly impedes cell cycle progression, induces apoptotic cell death, and impairs colony formation in ATC cells. THZ531 causes a loss of elongating RNA polymerase II and suppresses gene expression in ATC cells. An integrative analysis of gene expression profiles and super-enhancer landscape, combining with functional assays, leads to the discovery of two new ATC cancer genes, ZC3H4 and NEMP1. Furthermore, CDK12 inhibition enhances the sensitivity of ATC cells to doxorubicin-mediated chemotherapy. Thus, these findings indicate that CDK12 is a potential therapeutic target for ATC treatment and its inhibition may help to overcome the chemoresistance in patients with ATC

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Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma [ChIP-seq]

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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

Expression analysis of mouse thyroid tumors

Project description:Anaplastic thyroid carcinoma (ATC) is the most aggressive form of thyroid cancer, and often derives from pre-existing well-differentiated tumors. We have engineered the first mouse model of ATC by combining in the mouse thyroid follicular cells two molecular hallmarks of human ATC: activation of PI3K (via Pten deletion) and inactivation of p53. By 9 months of age, over 75% of the compound mutant mice develop aggressive, undifferentiated thyroid tumors that evolve from pre-existing follicular hyperplasia and carcinoma. These tumors display all the features of their human counterpart, including pleomorphism, epithelial-mesenchymal transition, aneuploidy, local invasion and distant metastases. We have performed expression profiling of thyroids from control, single mutants, compound mutants, follicular tumors from Pten-/- mice, and anaplastic tumors from Pten, p53-/- mice.

2012-03-14 | E-GEOD-30427 | biostudies-arrayexpress

Expression analysis of mouse thyroid tumors

2012-03-14 | GSE30427 | GEO

MiRNA Deregulation Distinguishes Anaplastic Thyroid Carcinoma (ATC) and Supports Upregulation of Oncogene Expression

Project description:Anaplastic thyroid carcinoma (ATC) is the most fatal and rapidly evolving endocrine malignancy invading the head and neck region and accounting for the majority of thyroid cancer-associated deaths. Deregulation of microRNA (miRNA) expression promotes thyroid carcinoma progression by modulating reorganization of the ATC transcriptome. Here, we applied comparative miRNA-/mRNA-sequencing in a cohort of 28 thyroid carcinomas to unravel the association of deregulated miRNA and mRNA expression. This identifies 85 miRNAs significantly deregulated in ATC. By establishing a new analysis pipeline we unravel 85 prime miRNA-mRNA interactions supporting the downregulation of candidate tumor-suppressors and upregulation of bona fide oncogenes like survivin (BIRC5) in ATC. This miRNA-dependent reprogramming of the ATC transcriptome provides a mRNA signature comprising 65 genes sharply distinguishing ATC from other thyroid carcinomas. Validation of deregulated protein expression in an independent thyroid carcinoma cohort demonstrates that miRNA-dependent oncogenes comprised in this signature, the transferrin receptor TFRC (CD71) and the E3-ubiquitin ligase DTL, are sharply upregulated in ATC. This upregulation is even sufficient to distinguish ATC from partially differentiated thyroid carcinomas (PDTC). In sum, these findings provide new diagnostic tools and a robust resource to explore key miRNA-mRNA regulation underlying the progression of thyroid carcinoma.

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