Transcription profiling of human medullary thyroid carcinoma cell line TT sunitinib or vehicle treatment time course
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER:
PROVIDER: E-TABM-929 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:RNA was extracted with Rneasy Micro Kit (Qiagen, France) from SKBR3 cells treated with 1 uM ATRA. The quantity and purity of the extracted RNA was evaluated using a NanoDropTM spectrophotometer and its integrity measured using an Agilent BioanalyzerTM. For microarray hybridizations, 500 ng of total RNA from each RNA sample was amplified and labeled with two fluorescents dye (Cy5 and Cy3) using the Quick Amplification Labeling kit (Agilent Technologies, Palo Alto, CA, USA) following the manufacturer's protocol. Cy3-labeled and Cy5-labelled cRNA were hybridized to the Agilent Human Whole Genome Oligo Microarray format 4x44K (Agilent Technologies), prior to washing and scanning.
2012-03-02 | E-MTAB-1013 | biostudies-arrayexpress
Project description:The mouse aldehyde oxidase, Aox4 (aldehyde oxidase 4), is a molybdo-flavoenzyme. Harderian glands are the richest source of Aox4, although the protein is detectable also in sebaceous glands, epidermis and other keratinized epithelia. We performed whole genome gene expression experiment on Harderian Gland, White Adipose Tissue and Liver of WT and Aox4-/- animals.
2015-09-15 | E-MTAB-3820 | biostudies-arrayexpress
Project description:Radiotherapy has a critical role in the treatment of small cell lung cancer (SCLC). Effectiveness of radiation in SCLC remains limited as resistance results from defects in apoptosis. In the current study, we investigated whether using a Bcl-2/Bcl-XL inhibitor S44563 can enhance radiosensitivity of SCLC cells in vitro and in vivo. In vitro studies confirmed that S44563 induce apoptosis in SCLC cells by inducing hallmarks of apoptosis (cleaved caspase-3, sub-G1 fraction induction and induction of the mitochondrial caspase activation pathway). S44563 markedly enhanced sensitivity of H146 cells and H69 cells to radiation in clonogenic assay. In addition, the combination S44563 and cisplatin-based chemo-radiation showed a dramatic tumor growth delay and increased overall survival in mouse xenograft models. In vitro experiments demonstrated a greater induction of apoptosis (sub-G1 fraction and cleaved caspase-3) with the combination as well as in vivo caspase-3 immunostaining. This positive interaction between S44563 and radiation was greater when S44563 was given after the completion of the radiation, which may be explained by the radiation-induced over expression of anti-apoptotic proteins (Bcl-2 and Bcl-XL) through the NF-?B pathway activation. Taken together, these data underline the critical role of sequence administration of targeted therapies with conventional therapies. SCLC cells which survive to IR highly rely on the induction of anti apoptotic proteins in part through NF- ?B activation for their survival yielding to the concept of 'contextual oncogene addiction' to the Bcl-2/Bcl-XL pathway providing rational for targeting survival pathways to potentiate IR. For transcriptome analysis, 106 cells were seeded in T25 flasks, allowed to growth for 24 h, and then left untreated or treated with 2 Gy radiation. After 24 hours, cells were harvested, lysed for the extraction of RNA, and processed to analyze gene expression.The design of this study consists to 6 hybridizations in dual color with Agilent Human Genome 4x44K (design 014850). The reference is always the untreated condition.
2013-02-01 | E-MTAB-966 | biostudies-arrayexpress
Project description:The IGR-Heu tumor cell line was established from patient Heu suffering from large cell carcinoma of the lung. Heu171, Heu127 and Heu161 T cell clones were isolated from autologous tumor infiltrating lymphocytes. H32 T cell line and H32-22 clone were isolated from autologous PBL after stimulation with IGR-Heu and sorting with peptide-MHC tetramers. T cells were grown in the presence of irradiated autologous tumor and lymphoblastoid cell lines in complete media supplemented with rIL-2 and conditioned medium from phytohemagglutinin-activated lymphocytes for 3 weeks. Then, for microarray assays, RNA was extracted from the different cells.
2007-03-02 | E-TABM-208 | biostudies-arrayexpress
Project description:Hypoxia-mediated inhibition of specific tumour cell lysis
2009-03-12 | E-TABM-611 | biostudies-arrayexpress
Project description:Characterize the genes deregulated in CD34 positive cells from peripheral blood of FPD/AML patients harbouring two different RUNX1 mutations. RUNX1 (also called AML1), a DNA-binding subunit of the CBF transcription factor family, is a master regulatory gene in hematopoiesis and acts as a tumour suppressor. Heterozygous germ line alterations in RUNX1 lead to a familial platelet disorder with a propensity to develop acute myeloid leukemia (FPD/AML). Although RUNX1 abnormalities per se are not sufficient to induce full-blown leukemia in FPD, this pathology represents a valuable model to understand how RUNX1 germ line mutations predispose to acquisition of additional genetic changes leading to leukemia transformation. To investigate how RUNX1 may predispose to leukemia, we performed a comparative study between two pedigrees harbouring different RUNX1 mutations, one associated with only thrombocytopenia (R139stop) and the other leading to thrombocytopenia and leukemic predisposition (R174Q).
2010-09-11 | E-TABM-792 | biostudies-arrayexpress
Project description:VHL is a tumor suppressor gene involved in the oxygen-sensing pathway whose germline mutations predispose to distinct phenotypes. Heterozygous mutations predispose to von Hippel-Lindau disease characterized by the development of multiple tumors (including hemangioblastomas, renal cell carcinomas and pheochromocytomas)1-3. More recently, a specific VHL-R200W mutation was shown to be responsible for Chuvash Polycythemia in homozygous carriers whereas heterozygous individuals have no clinical manifestation4. We report here a family carrying, on the same allele, VHL mutations characteristics of the two types of disease (a Chuvash polycythemia-R200W mutation and a von Hippel-Lindau disease-R161Q mutation). Genotyping, modeling analysis and functional studies, including transcriptomic profile of the distinct mutants validated for the first time on direct HIF target genes, show a gradual capacity of the VHL mutants to regulate the hypoxia responsive pathway that correlate with the severity of the developed phenotype. Our study provide original results that illuminate genotype/phenotype correlations in von Hippel-Lindau disease.
2013-09-03 | E-MTAB-1269 | biostudies-arrayexpress
Project description:Suppressor of cytokine signaling (SOCS1) is an inducible negative regulator of cytokine signaling. SOCS1 is expressed in normal colonic epithelium and colon adenocarcinomas. However, the levels of SOCS1 decreased during progression of colon adenocarcinomas, the lowest level being found in the more aggressive stage and least differentiated carcinomas. The restoration of SOCS1 in a colon cancer cell line induced expression of E-cadherin associated with disappearance of the mesenchymal form of the p120ctn. SOCS1 expression is sufficient to revert many characteristics of EMT. This reversion is dependent on the regulation of expression of the transcription factor ZEB1, both at transcriptional and translational levels. Furthermore, miRNA profiling indicates that SOCS1 also upregulates the expression of the mir-200 family of microRNAs, which can promote the mesenchymal-epithelial transition and reduce tumor cell migration. Expression of SOCS1 within the colon carcinoma cell lines dramatically reduced the invasive properties of the cells in vitro. This property was also observed in mice inoculated intracardially with SW620 cells where SOCS1 expression not only reduced the number of animals bearing metastases. Thus, SOCS1 up-regulates expression of E-cadherin to reduce colon cancer cells invasive properties. This pathway could be associated with colorectal cancer survival by reducing the capacity of generating metastases.This project concern 2 replicates in dye-swap of SW620 cells with and without transfected SOCS1 on a 244K custom human genomic expression microarray.
2014-05-01 | E-MTAB-1742 | biostudies-arrayexpress
Project description:Goal of the experiment Recurrence is a frequent phenomenon in intracranial childhood ependymomas. To understand this process, we investigated whether the gene expression profiling of matched ependymomas at diagnosis and at relapse could reveal key molecular events involved in tumor progression. To gain new insight in this process and identify pathways associated with recurrence, we compared the gene expression profiles of local recurrences with the corresponding initial tumors. Brief description We analyzed 17 tumor samples at diagnosis and a total of 27 paired recurrences. Recurrences analyzed occurred after surgery only in 12 cases, surgery plus chemotherapy only in 9 cases and any treatment plus radiotherapy in 6 cases. We compared the level of gene expression for each tumor at recurrence relative to its expression at diagnosis using Agilent 44K dual color gene expression microarrays.
2010-12-31 | E-TABM-873 | biostudies-arrayexpress
Project description:Docetaxel is used as a standard treatment in patients with metastatic castration-resistant prostate cancer. However, a large subset of patients develops resistance by mechanisms that remain largely unknown. It is thus important to define the relevant pathways implicated in docetaxel-resistance and validate predictive biomarkers that will allow approaches of personalized treatment. In this aim, we established resistant IGR-CaP1 prostate cancer cell lines to different doses of docetaxel (IGR-CaP1-R cell lines) and investigated gene expression profiles by microarray analyses. We generated a signature of 112 genes potentially implicated in docetaxel-resistance whose expression is highly modified (Fold change M-bM-^IM-% 5). Among these genes, significant modification of expression was observed among cell cycle components in the resistant cells. Hence, we focused on the role of the cell cycle regulator LZTS1 located on chromosome 8p which was under-expressed in all our docetaxel-resistant models. LZTS1 extinction was confirmed at the RNA and protein levels. DNA methylation analysis revealed a stretch of 20 highly methylated CpGs in the region encompassing the exon 1 of LZTS1 promoter in the docetaxel-resistant cells suggesting the existence of an epigenetic regulation of LZTS1 expression in the resistant cells. By using siRNA strategy, we found evidence that LZTS1 plays an important role in the acquisition of the resistant phenotype. In addition, immunohistochemical staining showed that LZTS1 protein was absent or down-regulated in 33% of diagnostic biopsies obtained in patients with metastatic castration-resistant prostate cancer. This heterogeneous labeling suggests that LZTS1 might constitute a predictive biomarker of response to docetaxel chemotherapy. Furthermore, as Cdc25C is a LZTS1 partner in the mitosis regulation, we observed that targeting of Cdc25C with the pharmacological Cdc25C inhibitor NSC 663284 specifically killed the docetaxel-resistant cells. These results strongly suggest that Cdc25C plays a role in docetaxel resistance and that Cdc25C might be a therapeutic target to overcome docetaxel resistance. Altogether our findings identify an important role of LZTS1 in developing docetaxel resistance in prostate cancer through its role in regulating phosphatase Cdc25C. The set of gene expression with 4x44K Agilent ( design 014850) correspond to 6 doses of docetaxel 2?5 to 200 ug/ml) in dual color and dye-swap versus the IGR-Cap1 cell line without docetaxel.
2013-06-30 | E-MTAB-1221 | biostudies-arrayexpress