Fbc13ce2-df00-4e62-927d-4ae6801d0d6a - samples
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ABSTRACT:
PROVIDER: EGAD00001011677 | EGA |
REPOSITORIES: EGA
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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:<p>We used massively parallel, paired-end sequencing of expressed transcripts (RNA-seq) to detect novel gene fusions in short-term cultures of glioma stem-like cells freshly isolated from nine patients carrying primary glioblastoma multiforme (GBM). The culture of primary GBM tumors under serum-free conditions selects cells that retain phenotypes and genotypes closely mirroring primary tumor profiles as compared to serum-cultured glioma cell lines that have largely lost their developmental identities.</p>
| phs000505 | dbGaP
Project description:mRNA-sequencing of thyroid cancer cell lines
| PRJNA961069 | ENA
Project description:The transport of molecules via exosomes is one of the factors involved in cancer development, and transferred molecules can serve as specific tumor biomarkers. The aim of the study was the LC MS/MS proteomic analysis of exosomes released by FTC and 8305C thyroid cancer cell lines, and reference Nthy-ori 3-1 normal thyroid follicular cells. A total of 1769 unique proteins were identified in the exosome samples. For exosomes derived from Nthy ori 3 1 cell the highest number of 1504 proteins was identified, while exosomes from thyroid carcinomas FTC and 8305C cell lines had 730 and 1304 identified proteins, respectively. For the identified proteins, gene ontology analysis was performed in terms of their cellular location, molecular function and involvement in biological processes. For proteins that only appeared in tumor derived FTC- and 8305C-derived exosomes, enriched categories were related to cancer progression and included cell adhesion and positive regulation of cell migration. Also, proteins related to protein N linked glycosylation, drug resistance, and cell response to NK and T cell cytotoxicity were among those unique proteins. Finally label free quantification (LFQ) was performed for identified differentially expressed proteins between all possible group parings. For exosomes from thyroid cancer cells, the most differentiating proteins included collagen alpha 2(I) chain, tenascin, matrix metalloproteinase 1, Interstitial collagenase and C type lectin domain family 11 member A. The obtained results broadened the knowledge about the role of exosomal proteins in thyroid cancer and indicated potential biomarkers for further evaluation in clinical conditions.
2023-10-19 | MSV000093152 | MassIVE
Project description:Background: thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Objective: to understand why many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiation. Methods: a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity was expressed conditionally in 8505C cells originating from an undifferentiated thyroid carcinoma. The consequences of the inhibition of TTF-1 activity in the cells expressing the antagonist on cell proliferation, mRNA and miRNA expression were analyzed. Results: we observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. By contrast, no significant change was observed in the miRNA population. Conclusion: the persistence of TTF-1 expression observed in most dedifferentiated human thyroid cancer cell lines is likely to be explained by the fact that TTF-1 activity is still required for proliferation of these tumor cells as demonstrated here in the 8505C cell line. Microarrays hybridizations were performed on human thyroid cancer cells 8505C expressing a TTF1 antagonist (Engr HD –Dox) versus non-expressing cells (Engr HD +Dox) and versus cells expressing the control protein (Engr HDm – Dox). After amplification and labelling, sample pairs were hybridized onto HS1100_Human_MI_ReadyArray (Microarrays Inc., Huntsville, AL, USA). The oligonucleotide set consists of 40,604 70-mer probes that were designed using a transcriptome-based annotation of exonic structure for genomic loci. Hybridizations were replicated with dye swap.
2015-06-15 | E-GEOD-58587 | biostudies-arrayexpress
Project description:Background: thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Objective: to understand why many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiation. Methods: a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity was expressed conditionally in 8505C cells originating from an undifferentiated thyroid carcinoma. The consequences of the inhibition of TTF-1 activity in the cells expressing the antagonist on cell proliferation, mRNA and miRNA expression were analyzed. Results: we observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. By contrast, no significant change was observed in the miRNA population. Conclusion: the persistence of TTF-1 expression observed in most dedifferentiated human thyroid cancer cell lines is likely to be explained by the fact that TTF-1 activity is still required for proliferation of these tumor cells as demonstrated here in the 8505C cell line. Microarrays miRNA hybridizations were performed on 8505c cells expressing a TTF1 antagonist (Engr HD âDox) versus non-expressing cells (Engr HD +Dox), on cells expressing the control protein (Engr HDm â Dox) versus non-expressing cells (Engr HDm + Dox), and on cell expressing the TTF1 antagonist (Engr HDâ Dox) versus the cells expressing the control protein (Engr HDmâ Dox). Hybridizations were replicated with dye swap.
2016-06-01 | E-GEOD-58243 | biostudies-arrayexpress
Project description:We established deep-coverage thyroid-specific spectral libraries encompassing over 12,000 proteins, including samples from nine types of thyroid primary and lymph node metastases tissues and fifty thyroid cancer cell lines.
2024-09-27 | PXD051051 |
Project description:RNA-seq of human thyroid cancer cell lines expressing sh-mirE-YAP or YAPS127A
| PRJNA814733 | ENA
Project description:We performed single-cell RNA sequencing (scRNA-seq) on 3 normal thyroid, 7 papillary thyroid cancer (PTC), and 5 anaplstic thyroid cancer (ATC) cases. We used scRNA-seq to analyze serirne/glycine metabolism in thyroid tumors.
2023-10-17 | GSE232237 | GEO