MYC drives resistance to PI3K/mTOR targeted inhibition (gene expression)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE25172 | GEO | 2011/08/31
SECONDARY ACCESSION(S): PRJNA142801
REPOSITORIES: GEO
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Project description:Gene expression signatures were measured after treatment of cells with 50nM BEZ235. Affymetrix HG-U133AV2 expression arrays were performed according to the manufacturer's directions using RNA extracted by Qiagen RNeasy from engineered human cell-lines grown for 72h in the presence of 50nM BEZ235 Resulting expression signatures where derived based on phenotypic properties(resistance to BEZ235) of the cells (enriched vs GFP/HR).
2011-08-30 | E-GEOD-25172 | biostudies-arrayexpress
Project description:Genomic copy-number changes were measured using 250K StyI SNP arrays after selection of cells to enrich for resistance to BEZ235. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted using Qiagen DNeasy from engineered human cell-lines.
2011-08-31 | GSE25170 | GEO
Project description:Genomic copy-number changes were measured using 250K StyI SNP arrays after selection of cells to enrich for resistance to BEZ235. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted using Qiagen DNeasy from engineered human cell-lines. Resulting alterations in copy numbers were calculated based on SNP intensities.
2011-08-30 | E-GEOD-25170 | biostudies-arrayexpress
Project description:Gene expression signatures were measured in logarithmic growing cultures Affymetrix HG-U133AV2 expression arrays were performed according to the manufacturer's directions using RNA extracted by Qiagen RNeasy from engineered human melanoma cells
2013-03-07 | GSE38007 | GEO
Project description:Pheochromocytomas (PCC) are mostly benign tumors, amenable to complete surgical resection. However, 10–17% of cases can become malignant, and once metastasized, there is no curative treatment for this disease. Given the need to identify effective therapeutic approaches for PCC, we evaluated the antitumor potential of the dual PI3K/mTOR inhibitor BEZ235 against these tumors. We employed an in vivo model of endogenous PCCs (MENX mutant rats), which closely recapitulate the human tumors. Mutant rats with PCCs were treated with 2 doses of BEZ235 (20 and 30 mg/kg), or with placebo, for 2 weeks. Treatment with BEZ235 induced cytostatic and cytotoxic effects on rat PCCs, which could be appreciated by both staining the tumors ex vivo with appropriate markers, and non-invasively by functional imaging (diffusion weighted-DW-MRI) in vivo. Transcriptomic analyses of tumors from rats treated with BEZ235 or placebo identified potential mediators of therapy response. Slc6a2, encoding the norepinephrine transporter (NET), was downregulated in a dose-dependent manner by BEZ235 in rat PCCs. Moreover, BEZ235 reduced Slc6a2/NET expression also in PCC cell lines (PC12, MPC, MTT). Studies of a BEZ235-resistant derivative of the MPC cell line (MPCR) confirmed that the reduction of NET expression associates with the response to the drug. Reduction of NET expression following BEZ235 treatment in vivo could be monitored by Positron Emission Tomography (PET) using a tracer targeting NET. Altogether, we demonstrate the efficacy of BEZ235 against PCC in vivo, and show that functional imaging can be employed to monitor the response of PCC to PI3K/mTOR inhibition therapy.
2016-11-03 | GSE83401 | GEO
Project description:NT2 cells were treated with DMSO (control) or 10uM Retinoic Acid (RA). Total RNA was isolated using TriReagent, and subsequent cleanup with RNeasy columns (Qiagen) according to the manufacturer's directions. Hybridizations were performed according to Affymetrix guidelines using the Human HG-U133A chip containing 22,500 unique genetic elements. Double-stranded cDNA was synthesized using Superscript II RT (Invitrogen). In vitro transcription labeling was performed with biotin labeled nucleotides using the Bioarray High Yield RNA Labeling Kit (ENZO). 20 ul of labeled RNA per sample was added to the hybridization cocktail, with a total of 15 ug hybridized to the chip (16 hours, 45C). RMA analysis was performed using Gene Traffic software (Iobion), where raw data for each hybridization was normalized, background corrected and filtered for signal intensity of 50 or greater in at least one comparison. Keywords: other
2005-10-18 | GSE2448 | GEO
Project description:HEK293 cells were transfected with control plasmid (pcDNAI/Neo;Invitrogen) or with the plasmid encoding HCaRG. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen). Chips HG-U133A: - Labeling protocol: Enzo BioArray HighYield RNA Transcript Labeling Kit. - Hybridization: According to the manufacturer's protocol (Affymetrix). - Scanner: GeneArray 2500. - Normalization: Employing GCOS software, chips were normalized using all probe sets scaling option and target signal at 500. Chips HG-U133 Plus 2.0: - Labeling protocol: GeneChip IVT Labeling Kit. - Hybridization: According to the manufacturer's protocol (Affymetrix). - Scanner: GeneChip Scanner 3000. - Normalization: Employing GCOS software, chips were normalized using all probe sets scaling option and target signal at 500. Keywords: parallel sample
2005-10-19 | GSE2555 | GEO
Project description:The goal of this experiment was to understand the changes in gene expression in the human basal-like breast cancer cell line HCC1143 following treatment with the MEK inhibitor Trametinib (T), PI3K/mTOR inhibitor BEZ235 (B), the BET inhibition JQ1 (JQ), Trametinib + JQ1 (TJ), or BEZ235 + JQ1(BJ), compared to a DMSO control (D). Samples were treated for 72hr and run in triplicate.
2017-05-30 | GSE82032 | GEO
Project description:NT2 cells were treated with DMSO (control) or 10uM Retinoic Acid (RA). Total RNA was isolated using TriReagent, and subsequent cleanup with RNeasy columns (Qiagen) according to the manufacturer's directions. Hybridizations were performed according to Affymetrix guidelines using the Human HG-U133A chip containing 22,500 unique genetic elements. Double-stranded cDNA was synthesized using Superscript II RT (Invitrogen). In vitro transcription labeling was performed with biotin labeled nucleotides using the Bioarray High Yield RNA Labeling Kit (ENZO). 20 ul of labeled RNA per sample was added to the hybridization cocktail, with a total of 15 ug hybridized to the chip (16 hours, 45C). RMA analysis was performed using Gene Traffic software (Iobion), where raw data for each hybridization was normalized, background corrected and filtered for signal intensity of 50 or greater in at least one comparison.
2008-06-12 | E-GEOD-2448 | biostudies-arrayexpress
Project description:Purpose: We aim to identify transcriptomic changes associated with EGFR-mediated epithelial to mesenchymal transition in carcinoma cells of the upper aerodigestive tract Method: Kyse30 and FaDu (ATCC, Manassas, VA, USA) were passaged in DMEM or RPMI, 10% FCS, 1% penicillin/streptomycin, 5% CO2 atmosphere at 37°C. Treatment with EGF (PromoCell PromoKine, Heidelberg, Germany), EpEX-Fc (Pan et al. PMID: 30261040) were conducted under serum-free conditions for 6h and 72h. Results: Kyse30 cells: At 6h/72h of treatment high-dose EGF (9nM) induced 612/1208 genes; low-dose EGF (1.8nM) induced 397/0 genes; EpEX-Fc (50nM) induced 137/2 genes; high-dose EGF (9nM) + EpEX (50nM) induced 291/0 genes FaDu cells: At 6h/72h of treatment high-dose EGF (9nM) induced 994/1536 genes; low-dose EGF (1.8nM) induced 671/4 genes; EpEX-Fc (50nM) induced 36/0 genes; high-dose EGF (9nM) + EpEX (50nM) induced 911/103 genes Conclusion: High- and low-dose EGF treatment in Kyse30 and FaDu cells differ with respect to short-term and long-term gene regulation. High-dose EGF, which is associated with induction of EMT, induces a higher number of differentially regulated genes (DEGs) after 6h and has a sustained strong regulatory capacity at 72h, when other treatmernts showed no DEGs.
2022-10-26 | GSE200421 | GEO