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Gene expression profiling during treatment of COLO205 cells with selumetinib

ABSTRACT: Gene expression profiling during treatment of COLO205 cells with selumetinib

PROVIDER: PRJNA712993 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13921975.fastq.gz	Fastqsanger.gz
	SRR13921976.fastq.gz	Fastqsanger.gz
	SRR13921977.fastq.gz	Fastqsanger.gz
	SRR13921978.fastq.gz	Fastqsanger.gz
	SRR13921979.fastq.gz	Fastqsanger.gz

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Gene expression profiling during treatment of COLO205 cells with selumetinib

Project description:Here, we investigate gene expression response of the BRAFV600E mutant cell line COLO205 to the MEK inhibitor selumetinib / AZD6244 / ARRY-142886. Although selumetinib causes long term G1 arrest, we observe cells stochastically entering the cell cycle without re-activation of ERK and initiation of a normal proliferative gene expression programme. Genes encoding DNA replication and repair factors are downregulated during G1 arrest, but many of these are transiently induced when cells escaping arrest enter S and G2. Nonetheless, mRNAs encoding key DNA replication factors including the MCM replicative helicase complex, PCNA and TIPIN remain at very low abundance.

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Project description:Here, we investigate focal amplification patterns in and around the BRAF locus in BRAFV600Emutant COLO205 cells that acquire resistance to the MEK inhibitor Sleumetinib / AZD6244 / ARRY-142886. We find that BRAF amplifications occur frequently in COLO205 cells during acquisition of selumetinib resistance and that BRAFamplifications pre-exist selumetinib treatment but occurs predominantly via de novo mutations

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Project description:MDA231, BT549, and SUM159PT basal-like breast cancer cell lines were transfected with non-targeting siRNA (siCONTROL), siRNA targeting DUSP4 (siDUSP4), or siCONTROL + 4 or 24 hr of 1uM selumetinib. Cells were harvested at 96 hr post-siRNA transfection. Data were Log2 RMA normalized. We sought to identify changes in gene expression after MEK inhibition, or after loss of DUSP4 function in breast cancer cell lines.

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Project description:Anti-tumor effect of the combination between 5-FU and selumetinib was treatment schedule-dependent in BRAF or KRAS mutant CRC cells. Treatment of 5-FU for 2 days followed by selumetinib for another 2 days exhibited synergism for cell viability, whereas single or reversely combined treatment showed antagonism Microarray analysis revealed the distinct groups of genes underlying the efficacy for schedule-dependent treatment.

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