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Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility

ABSTRACT: Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility

PROVIDER: PRJNA736692 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14779079.fastq.gz	Fastqsanger.gz
	SRR14779080.fastq.gz	Fastqsanger.gz
	SRR14779081.fastq.gz	Fastqsanger.gz
	SRR14779082.fastq.gz	Fastqsanger.gz
	SRR14779083.fastq.gz	Fastqsanger.gz

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Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (RNA-Seq)

Project description:Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (RNA-Seq)

| PRJNA736696 | ENA

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-Seq)

Project description:Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-Seq)

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Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression under hypoxic conditions

Project description:RNA-Seq of human endothelial cells treated with acriflavine (ACF) with or without hypoxia revealed massive changes on gene expression. These were non-randomly and potentially due to DNA topoisomerase inhibition rather than HIF inhibition. Surprisingly, in contrast to protein-coding genes, RNA-Seq yielded that an exceeding number of lncRNAs is upregulated.

2022-01-19 | GSE186297 | GEO

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression under hypoxic conditions

Project description:Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression under hypoxic conditions

| PRJNA773246 | ENA

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (RNA-Seq)

Project description:RNA-Seq of human endothelial cells treated with ACF revealed massive changes on gene expression. These were non-randomly and strongly conserved to murine lung endothelial cells potentially due to DNA topoisomerase inhibition rather than HIF inhibition. Surprisingly, in contrast to protein-coding genes, RNA-Seq yielded that an exceeding number of lncRNAs is upregulated, e.g. FENDRR, H19, HIF1α-AS1 and FLJ31356, whereas BOLA3-AS1 and MEG3 were strongly downregulated. ATAC-Seq demonstrated that ACF leads to strong changes on chromatin accessibility on lncRNA promoters.

2022-01-19 | GSE176555 | GEO

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-Seq)

2022-01-19 | GSE176554 | GEO

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-19 | GSE176556 | GEO

Trichophyton rubrum transcriptome in response to acriflavine

Project description:Purpose: The dermatophyte Trichophyton rubrum is an anthropophilic filamentous fungus that infects keratinized tissues and is the most common etiologic agent isolated in cases of human dermatophytoses. To better understand the molecular effects of stress responses and fungal adaptability, we evaluated the effects of acriflavine, a cytoxic drug, on T. rubrum transcriptome in a time-course assay using high-throughput RNA-seq technology. Results: RNA-seq generated approximately 200 million short reads that were mapped to the Broad Institute’s Dermatophyte Comparative Database before differential gene expression analysis. A subset of 490 genes modulated in response to stress caused T. rubrum exposure to acriflavine were identified. These genes are involved in various cellular processes such as oxidation-reduction reactions, transmembrane transport, metal ion binding, and pathogenicity. The genes involved in pathogenicity were down-regulated, suggesting that this drug interferes with virulence factors that allow the establishment and maintenance of host infection. Conclusion: The results obtained in this large-scale analysis provide insights into the molecular events underlying the stress responses of T. rubrum Acriflavine.

2015-03-05 | GSE40425 | GEO

Transcription profiling of topoisomerase I inhibitor irinotecan (CPT-11) sensitive, resistant, and reverted human neuroblastomas

Project description:We have established a neuroblastoma model resistant in vivo to the topoisomerase I inhibitor irinotecan (CPT-11, Camptothecin-11, CAMPTOSAR®) in order to study resistance to these agents acquired in a therapeutic setting. Common mechanisms of resistance were not involved in this model and we thus explored the gene expression signature associated with resistance by comparing the transcriptomes of sensitive, resistant, and reverted tumours using high-throughput DNA microarrays.

2008-01-26 | E-TABM-211 | biostudies-arrayexpress

Acriflavine inhibits the epithelial-to-mesenchymal transition in vitro in liver and pancreatic cancer cells (part of study on HepG2)

Project description:Background: Epithelial-to-mesenchymal transition (EMT) is considered an important driving mechanism behind aggressive cancer phenotype. This was recently challenged by the finding that cells can metastasize without undergoing EMT. However, the same studies confirmed the important role of the EMT program in drug resistance. The EMT program is largely dependent on the cell’s microenvironment. Acriflavine (ACF) is a heteroaromatic dye with antibacterial and antiviral effects. Recently, ACF was suggested as anticancer agent for its topoisomerase inhibitor activity. ACF further blocks the hypoxia-inducible factor (HIF) pathway, an important driver of cancer aggressiveness. How ACF works in cancer is however unknown. Aim: Identification of the working mechanism, molecular pathways and signaling of ACF in EMT cancer cells. To this end, three in vitro models were developed of EMT induction (human pancreatic cancer cells stimulated with TGF-b1, human pancreatic cancer cells stimulated with CoCl2, drug resistance against sorafenib in human liver cancer cells). Only the third model - drug resistance against sorafenib in HepG2 cells - is discussed in this GEO submission.

2017-03-08 | GSE82110 | GEO

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