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Homo sapiens

ABSTRACT: Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters, a time course study (study 1/2)

PROVIDER: PRJNA291429 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2569740.fastq.gz	Fastqsanger.gz
	SRR2569750.fastq.gz	Fastqsanger.gz
	SRR2569760.fastq.gz	Fastqsanger.gz
	SRR2569770.fastq.gz	Fastqsanger.gz
	SRR2569741.fastq.gz	Fastqsanger.gz

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Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters, a dosage study (study 2/2)

Project description:The purpose of this study, including this dosage series and another time course series, was to establish gene expression signatures representing the interaction of pathways deregulated by tumor promoting agents and pathways induced by DNA damage. Human lymphoblastoid TK6 cells were pretreated with the protein kinase C activating tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and exposed to UVC-irradiation. The time and dose-responsive effects of the co-treatment were captured with RNA-sequencing (RNA-seq) in two separate experiments. TK6 cells exposed to both TPA and UVC had significantly more genes differentially regulated than the theoretical sum of genes induced by either stress alone, thus indicating a synergistic effect on global gene expression patterns. Further analysis revealed that TPA+UVC co-exposure caused synergistic perturbation of specific genes associated with p53, AP-1 and inflammatory pathways important in carcinogenesis. The 17 gene signature derived from this model was confirmed with other PKC-activating tumor promoters including phorbol-12,13-dibutyrate, sapintoxin D, mezerein, (-)-Indolactam V and resiniferonol 9,13,14-ortho-phenylacetate (ROPA) with quantitative real-time PCR (QPCR). Here we show a novel gene signature that may represent a synergistic interaction in the tumor microenvironment that is relevant to the mechanisms of chemical induced tumor promotion.

2015-10-02 | GSE71520 | GEO

Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters, a time course study (study 1/2)

Project description:The purpose of this study, including this time course series and another dosage series, was to establish gene expression signatures representing the interaction of pathways deregulated by tumor promoting agents and pathways induced by DNA damage. Human lymphoblastoid TK6 cells were pretreated with the protein kinase C activating tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and exposed to UVC-irradiation. The time and dose-responsive effects of the co-treatment were captured with RNA-sequencing (RNA-seq) in two separate experiments. TK6 cells exposed to both TPA and UVC had significantly more genes differentially regulated than the theoretical sum of genes induced by either stress alone, thus indicating a synergistic effect on global gene expression patterns. Further analysis revealed that TPA+UVC co-exposure caused synergistic perturbation of specific genes associated with p53, AP-1 and inflammatory pathways important in carcinogenesis. The 17 gene signature derived from this model was confirmed with other PKC-activating tumor promoters including phorbol-12,13-dibutyrate, sapintoxin D, mezerein, (-)-Indolactam V and resiniferonol 9,13,14-ortho-phenylacetate (ROPA) with quantitative real-time PCR (QPCR). Here we show a novel gene signature that may represent a synergistic interaction in the tumor microenvironment that is relevant to the mechanisms of chemical induced tumor promotion.

2015-10-02 | GSE71519 | GEO

Project description:Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters

| PRJNA291426 | ENA

Homo sapiens

Project description:Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters, a dosage study (study 2/2)

| PRJNA291428 | ENA

CPD-seq map of UV damage formation in isolated human genomic DNA

Project description:UV-induced CPDs were mapped in isolated human genomic DNA following 80J/m2 of UVC irradiation

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UVDE-seq map of 6-4PP formation in normal human skin fibroblasts

Project description:UV-induced 6-4PPs were mapped in normal human skin fibroblasts following 500J/m2 of UVC irradiation

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Isolation of repaired chromatin of UVC-irradiated human skin fibroblasts

Project description:To further study and understand the DNA damage responses, we developed aniFOUND, a new method for capturing under native conditions the repaired DNA and the proteins associated with it after UVC irradiation. hTert-immortalised human skin fibroblasts were irradiated with 20 J/m2 UVC and the nascent DNA that resulted from the Unscheduled DNA Synthesis was specifically labeled with nucleotide analogues (EdU). This newly repaired/synthesized DNA together with the bound proteins were pulled-down with streptavidin beads. For negative controls we used both irradiated, but non-labelled samples (+UV/-EdU) and labelled, but not irradiated cells (-UV/+EdU). The pulldowns were eluted from the beads by boiling in 0.1 % SDS.

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Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.

Project description:Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer. Keywords: time course, ultraviolet irradiation, UV, erbB2, mouse skin The dorsal skin of adult female CD-1 mice was clipped one day before treatment and shaved on the day of treatment. DMSO or 4 mg AG825 dissolved in DMSO was applied topically to the shaved back of the mice 2 h prior to exposure to 10 kJ/m^2 UV or sham irradiation. The UV dose was approximately 30% UVA, 70% UVB and <1% UVC, with a total output of 470 uW/cm^2. Flash frozen skin was removed and total RNA expracted with TRIzol reagent (Invitrogen) and further purified with an RNeasy kit (Qiagen). Amplification, reverse-transcription, biotinylation, and hybridization were all carried out under standard conditions and procedures recommended by the manufacturer.

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Time-course RNA-Seq analysis of UVC exposed Ramazzottius varieornatus.

Project description:Time-course RNA-Seq analysis of Ramazzottius varieornatus exposed to UVC for up to 72 hours

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CPD-capture-seq map of CPD formation in UV-irradiated primary melanocytes, normal human skin fibroblasts and UV-irradiated genomic DNA

Project description:UV-induced CPDs were mapped in primary skin melanocytes or normal human skin fibroblasts following either UVC or UVB irradiation and in isolated human genomic DNA (naked DNA control) that was UVB or UVC irradiated. CPDs were mapped across the human genome using the CPD-capture-seq method and the resulting libraries were captured for ~4000 genomic regions of interest (~3 Mbp) of the human genome by the company Rapid Genomics prior to Illumina sequencing

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