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Transcriptomics analysis of KB-3-1 xenograft mice treated with cisplatin

ABSTRACT: Transcriptomics analysis of KB-3-1 xenograft mice treated with cisplatin

PROVIDER: PRJNA743026 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15014564_1.fastq.gz	Fastqsanger.gz
	SRR15014564_2.fastq.gz	Fastqsanger.gz
	SRR15014565_1.fastq.gz	Fastqsanger.gz
	SRR15014565_2.fastq.gz	Fastqsanger.gz
	SRR15014566_1.fastq.gz	Fastqsanger.gz

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Transcriptomics analysis of KB-3-1 xenograft mice treated with cisplatin

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Project description:Treatment-related DNA hypermethylation may play a role in creating drug resistant phenotypes by inactivating genes that are required for cytotoxicity, but there have been no genome-wide studies to systematically investigate methylation of individual genes following exposure to chemotherapy. We used microarrays and a pharmacologic unmasking protocol in isogenic cisplatin-sensitive and -resistant cell lines to identify genes that were down-regulated in cisplatin-resistant cells and could be re-activated by the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-Aza-dC). We identified several hundred genes that were down-regulated in each resistant cell line. Of these, 30 genes were common to > 2 cell lines, and/or reported to be down-regulated in previous studies. siRNA knockdown of two candidate genes increased cell viability with cisplatin treatment in sensitive parental cell lines Cisplatin-sensitive and -resistant SCC cells and KB and KB cisplatin-resistant clones (n=2) were split to low density and treated with freshly prepared 5 microM 5-Aza-dC dissolved in 50% acetic acid/50% PBS or were mock treated with the same volume of vehicle in the media for 5 days. Subsequently, RNA was extracted and hybridized on Affymetrix U133A microarrays. Signal intensity and statistical significance was established for each transcript, and a 2-fold decrease in signal in each paired sensitive/resistant cell line in combination with 1.5-fold increase after 5Aza-dC treatment was used to identify candidate genes.

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