UVR induced DNA-damage in Cutaneous Melanoma
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30941 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3093740.fastq.gz | Fastqsanger.gz | |||
| ERR3093740_1.fastq.gz | Fastqsanger.gz | |||
| ERR3093740_2.fastq.gz | Fastqsanger.gz | |||
| ERR3093750.fastq.gz | Fastqsanger.gz | |||
| ERR3093750_1.fastq.gz | Fastqsanger.gz |
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Project description:Nucleotide excision repair (NER) orchestrates the repair of helix distorting DNA damage, induced by both ultraviolet radiation (UVR) and cisplatin. There is evidence that the global genome repair (GGR) arm of NER is dysfunctional in melanoma and it is known to have limited induction in melanoma cell lines after cisplatin treatment. The aims of this study were to examine mRNA transcript levels of regulators of GGR and to investigate the downstream effect on global transcript expression in melanoma cell lines after cisplatin treatment and in melanoma tumours. One melanocyte, three primary melanoma (MM200, IgR3, Me4405) and two metastatic melanoma (Mel-RM and Sk-mel-28) cell lines were treated with cispltain and gene expression profile data collected at 0, 6 and 24 hours. Biological duplicates were treated and RNA was collected for each cell line at each timepoint. The duplicated were run sperately on the WGGEX beadarrays and the results of the duplicates averaged for publication. The transcript expression results were cubic spline normalised using BeadStudio 2.0 software (Illumina, USA), and the remaining analyses was performed using GeneSpring GX 11.0. To account for bias or skewing of expression results all the gene expression profiles and each individual gene were normalized to the median resulting in two way normalisation. For visualisation of the results the data was log transformed.
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Project description:Cutaneous and acral melanoma cross-OMICs reveals prognostic cancer drivers associated with pathobiology and ultraviolet exposure
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Project description:Ultraviolet (UV) radiation is a major source of skin damage. It is important to define the programmed gene expression change after UV exposure, particularly in the C57BL/6 lab mice model. Here we systematically analyze the acute gene expression change in mouse skin after UV exposure.
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Project description:During the treatment of cutaneous melanoma, the presence of radioresistance compromised the therapeutic effects of radiotherapy. Yet, the mechanism of radioresistance in melanoma still remains unclear. Bioinformatic analysis of the transcriptomic sequencing showed PURPL was top up-regulated genes in response to ionizing radiation (IR) treatment in melanoma cells. Loss of PURPL notably repressed melanoma cell viability, colony formation, migration and invasiveness which potentiated PURPL’s role in radioresistance of melanoma. Further, loss-of- and gain-of-function analysis indicated that PURPL repressed IR-induced DNA damage and apoptosis. Mechanistically, RNA pulldown was performed and BID was identified as the interacting protein partner of PURPL. As the core gene of the mitochondrial apoptosis pathway, BID could be cleaved by Caspase-8 to generate tBID, which promotes the permeability of the mitochondrial membrane and the release of cytochrome c. IR treatment promotes the interaction between BID and Caspase-8 which was further strengthened by the loss of PURPL. The in vivo assays further verified the in vitro findings. Collectively, our study supports the pro-radioresistance role of PURPL in melanoma by inhibiting the interaction between BID and Caspase-8, which may provide a novel target for clinical radiotherapy.
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