RNA-seq of anaplastic thyroid carcinoma cells (CAL62 and 8505c) after E2F7 silencing
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ABSTRACT:
PROVIDER: PRJEB41448 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4859170_1.fastq.gz | Fastqsanger.gz | |||
| ERR4859170_2.fastq.gz | Fastqsanger.gz | |||
| ERR4859171_1.fastq.gz | Fastqsanger.gz | |||
| ERR4859171_2.fastq.gz | Fastqsanger.gz | |||
| ERR4859172_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:ChIP-seq experiment was performed using an antibody against E2F7 in CAL62 anaplastic thyroid cancer cell line, in order to define the genomic regions bound by this transcription factor and exploit its genomic function in this cancer setting.
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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
Project description:ChIP-seq analysis against E2F7 in CAL62 anaplastic thyroid cancer cells
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Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of DDX19B gene In the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. DDX19B was selected because it has significantly different GCHs in the two cell lines: 1.64 in BCPAP and 6.03 in 8505C. The significantly more up- and down-regulated genes in the transfected 8505C than in the transfected BCPAP cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.
2017-03-25 | GSE97028 | GEO
Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of PANK2 gene In the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. PANK2 was selected because it has significantly different GCHs in the two cell lines: 44.64 in BCPAP and 3.61 in 8505C. The significantly more up- and down-regulated genes in the transfected BCPAP than in the transfected 8505C cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.
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Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of NEMP1 (TMEM194A) gene encoding a nuclear envelope protein in the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. NEMP1 was selected because it has significantly different GCHs in the two cell lines: 5.95 in BCPAP and 0.40 in 8505C. The significantly more up- and down-regulated genes in the transfected BCPAP than in the transfected 8505C cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.
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Project description:Laminin-5 gamma-2 (LAMC2) is highly expressed in anaplastic thyroid carcinoma and associated with tumor progression, migration and invasion by modulating signaling of EGFR LAMC2 was highly expressed in ATC samples and cell lines compared to normal thyroid tissues. Silencing LAMC2 by shRNA in ATC cells moderately inhibited cell growth in liquid culture and dramatically decreased growth in soft agar and in xenografts growing in immunodeficient mice. Silencing LAMC2 caused cell cycle arrest and significantly suppressed migration, invasion and wound healing of ATC cells. Rescue experiments by overexpressing LAMC2 in LAMC2 knockdown cells, reversed the inhibitory effects as shown by increased cell proliferation and colony formation. Microarray data demonstrated that LAMC2 shRNA significantly altered expression of genes associated with migration, invasion, proliferation and survival. Immunoprecipitation studies showed that LAMC2 was bound to EGFR in ATC cells. Silencing of LAMC2 partially blocked EGF-mediated activation of EGFR and its downstream pathway. Anaplastic thyroid carcinoma (ATC) is an aggressive malignancy having no effective treatment. Laminin subunit gamma-2 (LAMC2) is an epithelial basement membrane protein involved in cell migration and tumour invasion and might represent an ideal target for the development of novel therapeutic approaches for ATC. LAMC2 was highly expressed in ATC samples and cell lines compared to normal thyroid tissues. Silencing LAMC2 by shRNA in ATC cells moderately inhibited cell growth in liquid culture and dramatically decreased growth in soft agar and in xenografts growing in immunodeficient mice. Silencing LAMC2 caused cell cycle arrest and significantly suppressed migration, invasion and wound healing of ATC cells. Rescue experiments by overexpressing LAMC2 in LAMC2 knockdown cells, reversed the inhibitory effects as shown by increased cell proliferation and colony formation. Microarray data demonstrated that LAMC2 shRNA significantly altered expression of genes associated with migration, invasion, proliferation and survival. Immunoprecipitation studies showed that LAMC2 was bound to EGFR in ATC cells. Silencing of LAMC2 partially blocked EGF-mediated activation of EGFR and its downstream pathway. LAMC2 was highly expressed in ATC samples and cell lines compared to normal thyroid tissues. Silencing LAMC2 by shRNA in ATC cells moderately inhibited cell growth in liquid culture and dramatically decreased growth in soft agar and in xenografts growing in immunodeficient mice. Silencing LAMC2 caused cell cycle arrest and significantly suppressed migration, invasion and wound healing of ATC cells. Rescue experiments by overexpressing LAMC2 in LAMC2 knockdown cells, reversed the inhibitory effects as shown by increased cell proliferation and colony formation. Microarray data demonstrated that LAMC2 shRNA significantly altered expression of genes associated with migration, invasion, proliferation and survival. Immunoprecipitation studies showed that LAMC2 was bound to EGFR in ATC cells. Silencing of LAMC2 partially blocked EGF-mediated activation of EGFR and its downstream pathway. Anaplastic thyroid carcinoma cell lines (HTH83 and TL3) were infected with scrambled shRNA and LAMC2 shRNA and stable clones from each cell line were generated and used for RNA extraction and hybridization on Illumina Microarray. We compared scrambled shRNA stable cells with LAMC2 shRNA stable cells.
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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
Project description:Anaplastic thyroid carcinoma (ATC) has among the worst prognosis of any solid malignancy. The low incidence of the disease has in part precluded systematic clinical trials and tissue collection, and there has been little progress in developing effective therapies. BRAF and TP53 mutations co-occur in a high proportion of ATC, particularly those associated with a precursor papillary thyroid carcinoma (PTC). In order to develop an adult-onset model of BRAF-mutant anaplastic thyroid carcinoma, we generated a novel thyroid-specific CreER transgenic mouse. We utilize a Cre-regulated BrafV600E mouse and a conditional Trp53 allelic series to demonstrate that p53 constrains progression from papillary to anaplastic thyroid carcinoma. Gene expression and immunohistochemical analyses of murine tumors identified the cardinal features of human ATC including loss of differentiation, local invasion, distant metastasis and rapid lethality. We employed small animal ultrasound imaging to monitor autochthonous tumors, and show that treatment with the selective BRAF inhibitor PLX4720 improved survival, but did not lead to tumor regression or suppress signaling through the MAPK pathway. Combination of PLX4720 and the MEK inhibitor PD0325901 more completely suppressed MAPK pathway activation in mouse and human ATC cell lines, and improved the structural response and survival of ATC-bearing animals. This model expands the limited repertoire of autochthonous models of clinically aggressive thyroid cancer, and these data suggest that small molecule MAPK pathway inhibitors hold clinical promise in the treatment of advanced thyroid carcinoma. Total RNA from five murine papillary thyroid carcinoma (PTC) tumors and five murine anaplastic thyroid carcinoma (ATC) tumors was analyzed.
2014-04-02 | E-GEOD-55933 | biostudies-arrayexpress