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Transcriptome profiling of WM3248 melanoma cells following PGC1-alpha knockdown

ABSTRACT: Transcriptome profiling of WM3248 melanoma cells following PGC1-alpha knockdown

PROVIDER: PRJNA606044 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11067676.fastq.gz	Fastqsanger.gz
	SRR11067677.fastq.gz	Fastqsanger.gz
	SRR11067678.fastq.gz	Fastqsanger.gz
	SRR11067679.fastq.gz	Fastqsanger.gz
	SRR11067680.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of WM3248 melanoma cells following PGC1-alpha knockdown

Project description:PGC1-alpha is a transcriptional coactivator that controls diverse cellular processes, including metabolism. PGC1-alpha expression is increased in invasive primary melanoma. To understand the role of PGC1-alpha in the invasive growth of primary melanoma, we generated transcriptional (RNA-Seq) profiles of WM3248 primary melanoma cells that were transfected with either negative control or PGC1-alpha siRNA.

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PDGFR-alpha inhibits melanoma growth via CXCL10/IP-10 and miR-503. A multi-omics approach.

Project description:Cutaneous melanoma is the most aggressive skin cancer showing high mortality at advanced clinical stages. Platelet-Derived Growth Factor Receptor alpha (PDGFR-alpha) is known to strongly inhibit melanoma and endothelial cells proliferation, in vitro as well in vivo. PDGFR-alpha expression has been found to be reduced in metastatic human melanoma-biopsies, as compared to benign nevi-biopsies, thus implying a negative selection of PDGFR-alpha expressing cells, in melanoma. In the present study PDGFR-alpha was transiently overexpressed in endothelial (HUVEC) and melanoma (SK-Mel-28) human cells; a strong anti-proliferation effect was observed, along with profound effects on mRNA and miRNA expression. In detail, gene-expression profiling showed that PDGFR-alpha over-expression affects the expression of 82 transcripts in HUVEC (41 up-, 41 down-regulated), and 52 Transcripts in SK-Mel-28 (43 up-, 9 down-regulated). Finally, a miRNA profiling showed that 14 miRs are up-regulated and 39 are down-regulated in PDGFR-alpha overexpressing cells. Accurate validation with alternative techniques demonstrated that CXCL10 is one of the most significantly up-regulated at both gene- and protein level, in combination with a strong down-regulation of miR-503 in both HUVEC and SK-Mel-28 overexpressing PDGFR-alpha. We then demonstrate that CXCL10 is a validated miR-503 target, and that the anti-proliferation effect of PDGFR-alpha is reverted by specific CXCL-10 neutralization. In conclusion, PDGFR-alpha overexpression strongly inhibits endothelial- and melanoma- proliferation in a CXCL-10 dependent way, by significantly down-regulating miR-503 expression. This data set contains the results of the mRNA analysis.

2016-11-14 | E-MTAB-4261 | biostudies-arrayexpress

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