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Next Generation Sequencing of the transcriptomes of prostate cancer cells with or without ectopic expression of miR-5100

ABSTRACT: Next Generation Sequencing of the transcriptomes of prostate cancer cells with or without ectopic expression of miR-5100

PROVIDER: PRJNA1109812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28982878_1.fastq.gz	Fastqsanger.gz
	SRR28982878_2.fastq.gz	Fastqsanger.gz
	SRR28982879_1.fastq.gz	Fastqsanger.gz
	SRR28982879_2.fastq.gz	Fastqsanger.gz
	SRR28982880_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing of the transcriptomes of prostate cancer cells with or without ectopic expression of microRNA miR-30e

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Next Generation Sequencing of the transcriptomes of prostate cancer cells with or without ectopic expression of microRNA miR-30e

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Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.

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