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Human glioma cells treated with irradiation and/or CCI-779

ABSTRACT: Gene expression profiling of human glioma cell line LN-308. Cells were treated with the mTOR inhibitor CCI-779 or irradiated with a single dose of 4 Gy or a combination of both. The objective of this studywas to evaluate CCI-779 as a radio-sensitizing agent and to elucidate the underlying mechanisms.

ORGANISM(S): Homo sapiens

PROVIDER: GSE24232 | GEO | 2011/09/20

SECONDARY ACCESSION(S): PRJNA132927

REPOSITORIES: GEO

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Human glioma cells treated with irradiation and/or CCI-779

Project description:Gene expression profiling of human glioma cell line LN-308. Cells were treated with the mTOR inhibitor CCI-779 or irradiated with a single dose of 4 Gy or a combination of both. The objective of this studywas to evaluate CCI-779 as a radio-sensitizing agent and to elucidate the underlying mechanisms. Irradiated, CCI-779-, DMSO- (vehicle control) or combination treated LN-308 samples were hybridized against pooled untreated LN-308 samples as reference (CCI+Irradiation vs. Ref; CCI vs. Ref; DMSO+Irradiation vs Ref; DMSO vs. Ref).Three independent replicates were generated for each treatment and control, respectively.

2011-09-19 | E-GEOD-24232 | biostudies-arrayexpress

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Transcription profiling of mouse spinocerebellar ataxia type 3 (SCA3) transgenic and wild type animals treated with CCI-779 or placebo

Project description:Spinocerebellar ataxia type 3 is a neurodegenerative disorder caused by the expansion of the polyglutamine repeat region within the ataxin-3 protein. The mutant protein forms intracellular aggregates in the brain. However, the cellular mechanisms causing toxicity are still poorly understood and there are currently no effective treatments. In this study we show that administration of a rapamycin ester, CCI-779, improves motor performance in a transgenic mouse model of SCA3. CCI-779 inhibits mammalian target of rapamycin (mTOR) and hence upregulates protein degradation by autophagy. CCI-779 reduces the number of aggregates seen in the brains of transgenic mice and decreases levels of cytosolic soluble mutant ataxin-3, while endogenous wild-type protein levels remain unaffected. CCI-779 is designed for long-term use in patients and therefore represents a possible therapeutic strategy for the treatment of SCA3. Using this disease model and treatment paradigm we employed a microarray approach to investigate transcriptional changes that might be important in the pathogenesis of SCA3. This approach identified Usp15, which showed expression changes at both the mRNA and protein level. Usp15 levels were also changed in mice expressing another mutant polyglutamine protein, huntingtin. In total we identified 16 transcripts that were decreased in transgenic ataxin-3 mice that were normalised following CCI-779 treatment, as the number of transcripts changed was low and the magnitude of these changes was small we suggest that transcriptional dysregulation may not be an important step in the primary pathogenesis of SCA3. Experiment Overall Design: We analyzed 19 brain samples in total. 4 samples from wt animals after placebo treatment. 5 samples from wt animals after CCI-779 treatment. 5 samples from SCA3 tg animals after placebo treatment. 5 samples from SCA3 tg animals after CCI-779 treatment.

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Gene expression analysis of a MLL-rearranged leukaemia cell line, PER-485, treated with small molecule CCI-006.

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