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

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

PROVIDER: PRJNA773246 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16518291.fastq.gz	Fastqsanger.gz
	SRR16518292.fastq.gz	Fastqsanger.gz
	SRR16518293.fastq.gz	Fastqsanger.gz
	SRR16518294.fastq.gz	Fastqsanger.gz
	SRR16518295.fastq.gz	Fastqsanger.gz

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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 and chromatin accessibility

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

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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)

| PRJNA736697 | 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.

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DNA topoisomerase inhibition with the HIF inhibitor acriflavine promotes transcription of lncRNAs in endothelial cells.

Project description:The transcription factor hypoxia-inducible factor 1 (HIF1) is an important driver of cancer and is therefore an attractive drug target. Acriflavine (ACF) has been suggested to inhibit HIF1, but its mechanism of action is unknown. Here we investigated the interaction of ACF with DNA and long non-coding RNAs (lncRNAs) and its function in human endothelial cells. ACF promoted apoptosis and reduced proliferation, network formation, and angiogenic capacity. It also induced changes in gene expression, as determined by RNA sequencing (RNA-seq), which could not be attributed to specific inhibition of HIF1. A similar response was observed in murine lung endothelial cells. Although ACF increased and decreased a similar number of protein-coding genes, lncRNAs were preferentially upregulated under normoxic and hypoxic conditions. An assay for transposase accessibility with subsequent DNA sequencing (ATAC-seq) demonstrated that ACF induced strong changes in chromatin accessibility at lncRNA promoters. Immunofluorescence showed displacement of DNA:RNA hybrids. Such effects might be due to ACF-mediated topoisomerase inhibition, which was indeed the case, as reflected by DNA unwinding assays. Comparison with other acridine derivatives and topoisomerase inhibitors suggested that the specific function of ACF is an effect of acridinium-class compounds. This study demonstrates that ACF inhibits topoisomerases rather than HIF specifically and that it elicits a unique expression response of lncRNAs.

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Project description:Hypoxia-inducible factor (HIF)-1α is constitutively expressed in melanoma cells under normoxic conditions and its elevated expression correlates with the aggressiveness of melanoma tumors. Here, we used acriflavine, a potent inhibitor of HIF-1α dimerization, as a tool to investigate whether HIF-1α-regulated pathways contribute to the growth of melanoma cells under normoxia. We observed that acriflavine differentially modulated HIF-1α-regulated targets in melanoma under normoxic conditions, although acriflavine treatment resulted in over-expression of vascular endothelial growth factor (VEGF), its action clearly downregulated the expression of pyruvate dehydrogenase kinase 1 (PDK1), a well-known target of HIF-1α. Consequently, downregulation of PDK1 by acrifavine resulted in reduced glucose availability and suppression of the Warburg effect in melanoma cells. In addition, by inhibiting the AKT and RSK2 phosphorylation, acriflavine also avoided protective pathways necessary for survival under conditions of oxidative stress. Interestingly, we show that acriflavine targets activating transcription factor 4 (ATF4) for proteasomal degradation while suppressing the expression of microphthalmia-associated transcription factor (MITF), a master regulator of melanocyte development and a melanoma oncogene. Since acriflavine treatment results in the consistent death of melanoma cells, our results suggest that inhibition of HIF-1α function in melanoma could open new avenues for the treatment of this deadly disease regardless of the hypoxic condition of the tumor.

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Aspergillus CEA10 compared to SRBA mutant under hypoxic conditions

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Project description:To investigate the effects of hypoxia on osteocytes, we cultured MLO-Y4 osteocytic cells under normoxic (20% O₂) and hypoxic (2% O₂) conditions. We then performed gene expression profiling analysis using RNA-seq data obtained from these cells. Differential expression analysis revealed that Lipocalin 2 (LCN2) was one of the most significantly upregulated genes under hypoxic conditions.The dataset provides insights into the transcriptional response of osteocytes to hypoxic stress.

2025-05-30 | GSE298138 | GEO

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