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MYC drives resistance to PI3K/mTOR targeted inhibition (gene expression)

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE25172 | GEO | 2011/08/31

SECONDARY ACCESSION(S): PRJNA142801

REPOSITORIES: GEO

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MYC drives resistance to PI3K/mTOR targeted inhibition (gene expression)

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

MYC drives resistance to PI3K/mTOR targeted inhibition (Sty SNP array)

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.

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MYC drives resistance to PI3K/mTOR targeted inhibition (Sty SNP array)

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Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF

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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.

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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.

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