Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18899900.fastq.gz | Fastqsanger.gz | |||
| SRR18899901.fastq.gz | Fastqsanger.gz | |||
| SRR18899902.fastq.gz | Fastqsanger.gz | |||
| SRR18899903.fastq.gz | Fastqsanger.gz | |||
| SRR18899904.fastq.gz | Fastqsanger.gz |
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Project description:The E6 and E7 proteins are the major oncogenic drivers encoded by high-risk human papillomaviruses (HPVs). While many aspects of the transforming activities of these proteins have been extensively studied, there are fewer studies that have investigated how HPV E6/E7 expression affects expression of cellular noncoding RNAs. The goal of our study was to investigate HPV16 E6/E7 modulation of cellular microRNA (miR) levels and to determine the potential consequences on cellular gene expression. We performed deep sequencing of small and large cellular RNAs in primary, undifferentiated cultures of human foreskin keratinocytes (HFKs) with stable expression of HPV16 E6/E7 or a control vector. After integration of the two data sets we identified 51 differentially expressed cellular miRs associated with modulation of 1,456 potential target mRNAs in HPV16 E6/E7 expressing HFKs. We discovered that the degree of differential miR expression in HFKs expressing HPV16 E6/E7 was not necessarily predictive of the number of corresponding mRNA targets or the potential impact on gene expression. Additional analyses of the identified miR-mRNA pairs suggest modulation of specific biological activities and biochemical pathways. Overall, our study supports the model that perturbation of cellular miR expression by HPV16 E6/E7 importantly contributes to the rewiring of cellular regulatory circuits by the high-risk HPV E6 and E7 proteins that contribute to oncogenic transformation.
2017-01-17 | GSE92496 | GEO
Project description:Human papillomavirus (HPV) genome integration into the host genome, blocking E2 expression and leading to overexpression of E6 and E7 viral oncogenes, is considered a major step in cervical cancer development. In high-risk HPVs, E6 and E7 oncogenes are expressed as a bicistronic pre-mRNA, with alternative splicing producing the ultimate mRNAs required for E6 and E7 translation. Given the number of alternative donor and acceptor splicing sites, ten E6/E7 different alternative transcripts might be formed for HPV16 and three for HPV18, although only six isoforms have been previously reported for HPV16. In the present work, we employ high-throughput sequencing of invasive cervical cancer transcriptome (RNA-Seq) to characterize the expression of the HPV genome in 24 invasive cervical cancers associated with HPV16 and HPV18 single infections. Based on high-resolution transcriptional maps, we herein report three viral gene expression patterns which might be associated with the presence of the viral genome in episomal and/or integrated stages. Alternative mRNAs splicing isoforms coding for E6 and E7 oncoproteins were characterized and quantified, and two novel isoforms were identified. Three major isoforms (E6*I, E6*II, and E6+E7) were detected for HPV16 and two for HPV18 (E6*I and E6+E7). Minor transcript isoforms, including the novel ones, were very rare in some tumor samples or were not detected. Our data suggested that minor transcript isoforms of E6/E7 do not play a relevant role in cervical cancer.
2019-08-06 | GSE91065 | GEO
Project description:HPV E6 from the genus alpha 'high risk' types such as HPV16 recruit the ubiquitin ligase E6AP to ubiquitinate p53 and target it for proteasome-mediated degradation. This results in the functional inactivation of p53 in HPV16-E6 expressing cells. To test what patterns in gene expression might change as a result of HPV16 E6 protein functions and to test whether HPV E6 proteins from genus beta virus types also inactivate p53, we profiled gene expression using Affymetrix arrays before and after stimulating p53 activity via DNA damage in a panel of N/Tert-E6 cell lines.
2013-09-05 | GSE50568 | GEO
Project description:Comparative analysis of RNA expression profiles of keratinocytes expressing E6/E7 from the different beta-3, with the RNA profiles of HPV16 and HPV38 E6/E7 HFKs reveals that HPV115 is the more divergent from the HR-mucosal type. Moreover beta-3 HPV 49, 75 and 76 E6/E7 HFKs show altered expression of genes involved in cell cycle regulation and DNA damage response which are also deregulated by expression of E6/E7 of HPV16.
2020-07-04 | GSE100681 | GEO
Project description:Identification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes Keywords: ordered
2013-11-27 | GSE14051 | GEO
Project description:HPV E6 from the genus alpha 'high risk' types such as HPV16 recruit the ubiquitin ligase E6AP to ubiquitinate p53 and target it for proteasome-mediated degradation. This results in the functional inactivation of p53 in HPV16-E6 expressing cells. To test what patterns in gene expression might change as a result of HPV16 E6 protein functions and to test whether HPV E6 proteins from genus beta virus types also inactivate p53, we profiled gene expression using Affymetrix arrays before and after stimulating p53 activity via DNA damage in a panel of N/Tert-E6 cell lines. N/Tert-1 human keratinocyte cell lines were cultured in K-SFM (Invitrogen) and treated with 2 ug/ml mitomycin C or with vehicle control for 18 hours. RNA isolated from frozen cell pellets was analyzed on Affymetrix arrays. Each cell line was grown and processed on arrays in 3-5 separate experiments.
2013-09-05 | E-GEOD-50568 | biostudies-arrayexpress
Project description:This analysis aimed to identify differentially expressed genes in non-tumorigenic keratinocytes transduced with E6/E7 oncogenes of HPV16 or 18. The working cell models were named HaCaT E6/E7 HPV16, HaCaT E6/E7 HPV18, and HaCaT pLVX (empty lentiviral vector) as controls. mRNA sequencing was performed on the Illumina NovaSeq 6000 platform by Novogene Bioinformatics Technology Co., Ltd, Beijing, China, with two independent replicate sequences for each cell model. Methodology: The bioinformatics pipeline analysis was executed as described below: Rstudio (v2023.06.1+524) and Galaxy (https://www.usegalaxy.orgaccessed on 15 August 2023) open-source platforms were used to analyze the Illumina raw data. The Quality Check was performed through the FastQC tool (v0.12.1); afterward, all the reads were processed by the Rsubread package (v2.14.2); at that point, the reads were trimmed and aligned to the Human Genome Reference (GRCh38.p14 v43). The resulting output was the BAM files, of which the number of reads was counted by the featureCounts tool (v2.0.3); at the final step, the Differential Expression Analysis was settled by DESeq2 tool (v2.11.40.8). The differential gene expression measurements were normalized by DESeq2´s median of ratios (median of ratio of gene counts relative to geometric mean per gene) method. All chemokine genes with an adjusted p-value (adj p) ≤ 0.05 and fold change (Log2FC) > 1 .5 or < -1.5 were selected as differentially expressed genes (DEGs). Some genes from the resulting outputs were validated through qPCR. Conclusions: Our study found 3296 differentially expressed genes in HaCaT E6/E7 HPV16 and 1943 in HaCaT E6/E7 HPV18. These results suggest that E6/E7 oncogenes from HPV16 and 18 can broadly modify transcriptomic expression.
2023-11-02 | GSE241704 | GEO
Project description:We analyzed the effects of the expression of HPV 16 E6 oncoprotein variants (AA-a, AA-c, E-A176/G350, E-C188/G350, E-G350), and the E- Prototype in global gene expression profiles in an in vitro model. E6 gene was cloned into an expression vector fused to GFP and was transfected in C33-A cells. Affymetrix GeneChip Human Transcriptome Array 2.0 platform was used to analyze the expression of over 245,000 coding transcripts. We found that HPV16 E6 variants altered the expression of 431 genes in comparison with EPrototype. The altered genes are involved in cellular processes related to the development of cervical carcinoma, such as adhesion, angiogenesis, apoptosis, differentiation, cell cycle, proliferation, transcription and protein translation. Our results show that polymorphic changes in HPV16 E6 natural variants are sufficient to alter the overall gene expression profile in C33-A cells, explaining in part the observed differences in oncogenic potential of HPV16 variants.
2015-11-20 | GSE73761 | GEO
Project description:The infection with high-risk human papillomavirus is aetiologically linked to cervical cancer, the role of miRNAs regulated by virus oncogene in cancer progression remain largely unknown. Here, we screened the differentially expressed miRNAs with miRNA array between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines In the study, we screened the differentially expressed miRNAs with miRNA array (Exiqon, miRCURY LNA microRNA array, 7th gen [hsa, miRBase 18]) between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines to found miRNAs regulated by virus oncogene e6/e7. Biological replicates: 3 control, 3 e6/e7 silenced, independently grown and harvested. four replicates per array.
2016-07-01 | E-GEOD-68153 | biostudies-arrayexpress
Project description:Identification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes Keywords: ordered We used microarrays to identify differentially expressed genes in human foreskin keratinocytes (HFK) transfected with retroviral vectors harboring the human papillomavirus type 16 oncogenes E6, E7, or E6/E7 in comparison to HFK containing the empty vector control pLXSN.
2013-11-27 | E-GEOD-14051 | biostudies-arrayexpress