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Comparison of gene expression alterations induced by distinct PI3K inhibitors

ABSTRACT: The goal is the characterization of the off-target activity of BKM120 observed in A2058 human melanoma cell line at IC90 concentration (3.606 µM) but not at lower concentrations. Controls are BEZ235, GDC0941, showing no off-target activity. A secondary objective is the characterizations of drug effects on transcript expression with respect to a control treatment (DMSO) of those PI3K inhibitors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33643 | GEO | 2012/07/01

SECONDARY ACCESSION(S): PRJNA148663

REPOSITORIES: GEO

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Comparison of gene expression alterations induced by distinct PI3K inhibitors

Project description:The goal is the characterization of the off-target activity of BKM120 observed in A2058 human melanoma cell line at IC90 concentration (3.606 ÂµM) but not at lower concentrations. Controls are BEZ235, GDC0941, showing no off-target activity. A secondary objective is the characterizations of drug effects on transcript expression with respect to a control treatment (DMSO) of those PI3K inhibitors. 3 compounds, 3 concentrations per compound treatment, DMSO control treatement, 4 biological replicates

2012-06-30 | E-GEOD-33643 | biostudies-arrayexpress

Gene expression signatures of JBV cells treated with miR-145

Project description:To examine the difference of gene expression profiles between malignant melanoma cells treated with neopetasin (NP), metformin (Met), and phenformin (Phen), we have employed microarray expression profiling as a discovery platform. A2058 (human malignant melanoma) cells were treated for 8 hours with NP (3 µM), Met (5,00 µM), and Phen (50 µM).

2023-09-27 | GSE214209 | GEO

Gene expression signatures of A2058 cells treated with neopetasin, metformin, and phenformin

2021-09-09 | GSE150348 | GEO

Targeting PI3K/mTOR signaling exerts potent antitumor activity in pheochromocytoma in vivo

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

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 (gene expression)

2011-08-31 | GSE25172 | GEO

mTOR inhibitors synergistically induce regression, reversal of gene expression and autophagy in hepatocellular carcinoma

Project description:The mTOR-allosteric inhibitor, RAD001, in combination with a PI3K/mTOR ATP-site competitive inhibitor, BEZ235, causes gene reprogramming, autophagy and tumor regression, in a mouse model approximating human HCC with poor prognosis, leading to an investigator Phase 1B-2 clinical trial. Comparative study of total RNA obtained from normal and tumor liver tissue under RAD001, BEZ235, or RAD001 + BEZ235.

2012-07-11 | E-GEOD-37129 | biostudies-arrayexpress

Identification of early targets of SOX2 and PI3K signaling in normal, patient-derived tracheal basal cell lines.

Project description:Microarrays were used to examine gene expression changes in patient derived tracheal basal cell lines after treatment with Lenti-SOX2. Comparisons were made between baseline, Lenti-SOX2 and Lenti-SOX2 with a PI3K inhibitor (BKM120). Total RNA obtained from celll lnes 36 hours post lentivirus addition.

2015-07-01 | E-GEOD-59866 | biostudies-arrayexpress

Identification of early targets of SOX2 and PI3K signaling in normal, patient-derived tracheal basal cell lines.

2015-07-01 | GSE59866 | GEO

Human basal-like breast cancer cell line HCC1143 treated with BET inhibitor JQ1 in combination with MEK inhibitor Trametinib or PI3K/mTOR inhibitor BEZ235

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

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