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

ABSTRACT: 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.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE176555 | GEO | 2022/01/19

REPOSITORIES: GEO

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Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-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 | GSE176554 | GEO

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

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

Acriflavine inhibits the epithelial-to-mesenchymal transition in vitro in liver and pancreatic cancer cells (part of study with TGF-b1 stimulation)

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 first model - PANC1 stimulated with TGF-b1 - is discussed in this GEO submission.

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Long Noncoding RNA HNF1A-AS1 Regulates Proliferation and Migration in Esophageal Adenocarcinoma Cells

Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair

2013-10-21 | E-GEOD-48240 | biostudies-arrayexpress

Acriflavine inhibits the epithelial-to-mesenchymal transition in vitro in liver and pancreatic cancer cells (part of study on PANC1 cells treated with CoCl2)

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 second model - PANC1 with CoCl2, a model of severe hypoxia - is discussed in this GEO submission.

2017-03-08 | GSE82104 | GEO

The aberrant inclusion of BOLA3 exon 3 promoted by HNRNPC acts as an oncogenic driver in esophageal squamous cell carcinoma [11pairs RNA-seq]

Project description:Aberrant RNA splicing events produce transcripts to facilitate ESCC progression, yet how this splicing process is abnomally regulated remains elusive. Here, we unveil a alternative splicing axis of BOLA3 transcripts and its regulator HNRNPC in ESCC.The long isoform of BOLA3 (-L) with exon3 is highly expressed in ESCC and associated with poor prognosis. Functional assays demonstrate the pro-tumorigenic function of BOLA3-L in ESCC cells. HNRNPC binds to BOLA3-L pre-mRNA and promotes exon3 inclusion forming BOLA3-L. HNRNPC knockdown suppresses the tumorigenesis of ESCC cells, phenocopying BOLA3-L knockdown, which is significantly rescued by BOLA3-L overexpression. High expression of HNRNPC is correlated with the exon-3 inclusion of BOLA3 in ESCC and associated with poor prognosis. BOLA3-L maintains mitochondrial structural and functional stability, exerting pro-oncogenic effects through the WNT/β-catenin pathway. E2F7 acts as a key transcription factor to regulate the transcriptional upregulation of HNRNPC and promotes the inclusion of BOLA3 exon3.Taken together, our findings provide insights into how alternative splicing contributes to ESCC progression, by investgating a HNRNPC-BOLA3 splicing axis.

2024-01-01 | GSE235537 | GEO

The aberrant inclusion of BOLA3 exon 3 promoted by HNRNPC acts as an oncogenic driver in esophageal squamous cell carcinoma [shHNRNPC RNA-seq]

2024-01-01 | GSE235536 | GEO

The aberrant inclusion of BOLA3 exon 3 promoted by HNRNPC acts as an oncogenic driver in esophageal squamous cell carcinoma [shBOLA3-L RNA-seq]

2024-01-01 | GSE235535 | GEO

Analysis of the early transcriptome signature of Nipah virus infection in primary endothelial cells

Project description:Nipah virus (NiV) is a recently emerged zoonotic Paramyxovirus that causes regular outbreaks in East Asia with mortality rate exceeding 75%. Major cellular targets of NiV infection are endothelial cells and neurons. To better understand virus-host interaction, we analysed the transcriptome profile of NiV infection in primary human umbilical vein endothelial cells. We found that NiV infection strongly induces genes involved in interferon response in endothelial cells. Among the top ten upregulated genes, we identified the chemokine CXCL10 (interferon-induced protein 10, IP-10), an important chemoattractant involved in the generation of inflammatory immune response and neurotoxicity. We performed microarray gene expression profiling of NiV infected HUVEC cell (2 replicates) and of uninfected HUVEC cell (2 replicates).

2012-08-24 | E-GEOD-32902 | biostudies-arrayexpress

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