Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1177673 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31113063_1.fastq.gz | Fastqsanger.gz | |||
| SRR31113063_2.fastq.gz | Fastqsanger.gz | |||
| SRR31113064_1.fastq.gz | Fastqsanger.gz | |||
| SRR31113064_2.fastq.gz | Fastqsanger.gz | |||
| SRR31113065_1.fastq.gz | Fastqsanger.gz |
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Project description:Metformin has been shown to downregulate viral E6/E7 expression in HPV-positive cancer cells. However, Metformin does not induce cellular senescence, which is observed upon E6/E7 repression by RNA interference. Here we compare mass spectrometry-based proteome analyses of Metformin-treated SiHa cells (previously deposited to the ProteomeXchange Consortium with data set identifier PXC011095) with proteome analyses of SiHa cells transfected with si16E6/E7 or control siRNA (siCtrl-1) and grown for 72 hours to evaluate differences in the cell cycle regulation of HPV-positive cancer cells upon E6/E7 repression by Metformin or siE6/E7.
2025-06-17 | PXD061861 | Pride
Project description:The life cycle of human papillomaviruses (HPV) is strictly linked to the differentiation of their natural host cells. The HPV E6 and E7 oncoproteins can delay the normal differentiation program of keratinocytes, however, the exact mechanisms responsible for this have not yet been identified. The goal of this study was to investigate the effects of HPV16 oncoproteins on the expression of genes involved in keratinocyte differentiation. Primary human keratinocytes transduced by LXSN (control) retroviruses or virus vectors expressing HPV16 E6, E7 or E6/E7 genes were subjected to gene expression profiling. The results of microarray analysis showed that HPV 16 E6 and E7 have the capacity to down-regulate the expression of several genes involved in keratinocyte differentiation. Quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to confirm microarray data. To investigate the effects of the HPV oncoproteins on the promoters of selected keratinocyte differentiation genes, luciferase reporter assays were performed. Our results suggest that the HPV 16 E6 and/or E7 oncogenes are able to down-regulate the expression of several genes involved in keratinocyte differentiation, at least partially by down-regulating their promoter activity. This activity of the HPV oncoproteins may have a role in the productive virus life cycle, and also in virus induced carcinogenesis. Primary human foreskin keratinocytes were transduced by retrovirus vectors containing HPV 16 E6, E7, E6/E7 or the control vector LXSN. The global gene expression patterns of transduced keratinocytes were analyzed on Affymetrix microarrays
2014-06-26 | E-GEOD-58841 | biostudies-arrayexpress
Project description:Human papillomavirus (HPV) E6 and E7 oncoproteins are expressed at all stages of HPV-mediated carcinogenesis and are essential drivers of cancers caused by high-risk HPV. Some of the activities of HPV E6 and E7, such as their interactions with host cellular tumor suppressors, have been characterized extensively. There is less information about how high-risk HPV E6 and E7 alter cellular responses to cytokines that are present in HPV-infected tissues and are an important component of the tumor microenvironment. We used several models of HPV oncoprotein activity to assess how E6 and E7 alter the cellular response to the pro-inflammatory cytokine IL-1beta. Models of early-stage HPV infection (human keratinocytes expressing HPV16 E6 and E7) and models of established HPV-positive head and neck cancers (patient-derived xenografts, head and neck cancer cell lines) exhibited similar dysregulation of IL-1 pathway genes and suppressed responses to IL-1beta treatment. Such overlap in cell responses supports that changes induced by HPV E6 and E7 early in infection could persist and contribute to a dysregulated immune environment throughout carcinogenesis. HPV E6 and E7 also drove the upregulation of several suppressors of IL-1 cytokine signaling, including SIGIRR, both in primary keratinocytes and in cancer cells. SIGIRR knockout was insufficient to increase IL-1beta-dependent gene expression in the presence of HPV16 E6 and E7, suggesting that multiple suppressors of IL-1 signaling contribute to dampened IL-1 responses in HPV16-positive cells.
2022-10-31 | GSE211730 | GEO
Project description:The life cycle of human papillomaviruses (HPV) is strictly linked to the differentiation of their natural host cells. The HPV E6 and E7 oncoproteins can delay the normal differentiation program of keratinocytes, however, the exact mechanisms responsible for this have not yet been identified. The goal of this study was to investigate the effects of HPV16 oncoproteins on the expression of genes involved in keratinocyte differentiation. Primary human keratinocytes transduced by LXSN (control) retroviruses or virus vectors expressing HPV16 E6, E7 or E6/E7 genes were subjected to gene expression profiling. The results of microarray analysis showed that HPV 16 E6 and E7 have the capacity to down-regulate the expression of several genes involved in keratinocyte differentiation. Quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to confirm microarray data. To investigate the effects of the HPV oncoproteins on the promoters of selected keratinocyte differentiation genes, luciferase reporter assays were performed. Our results suggest that the HPV 16 E6 and/or E7 oncogenes are able to down-regulate the expression of several genes involved in keratinocyte differentiation, at least partially by down-regulating their promoter activity. This activity of the HPV oncoproteins may have a role in the productive virus life cycle, and also in virus induced carcinogenesis.
2014-06-26 | GSE58841 | GEO
Project description:In the preset study we isolated and characterized exosomes from both HPV positive and negative cervical cancer cell lines and identified a subset of mRNA’s enriched specifically in HPV positive exosomes through deep sequencing methods. Potential target prediction gene ontology, KEGG pathway analysis revealed possible functions associated with differentially expressed genes of CaCx exosomes. Profiling of these exosomes also revealed the export of HPV 16 associated transcripts (E1,E2, E5, and L2) within SiHa exosomes, however no such export was observed for major oncogenic transcripts (E6 and E7). Our Reverse transcription PCR experiments could validate our deep sequencing results for the absence of E6, E7 transcripts in exosomes. Interestingly, PCR could amplify a truncated version of E6 transcript in HeLa exosomes, which was not detectable in our sequencing results.
2022-06-01 | GSE161875 | GEO
Project description:Specific types of human papillomaviruses (HPVs) cause cervical cancer, the second most common tumor in females worldwide. Both cellular transformation and the maintenance of the oncogenic phenotype of HPV-positive tumor cells are linked to the expression of the viral E6 and E7 oncogenes. In order to identify downstream cellular target genes for the viral oncoproteins, we silenced endogenous E6 and E7 expression in HPV-positive HeLa cells by RNA interference (RNAi). Subsequently, we assessed changes of the cellular transcriptome by genome-wide microarray analysis. We identified, 648 genes wich were either downregulated (360 genes) or upregulated (288 genes) upon inhibition of E6/E7 expression. A large fraction of these genes is involved in tumour-relevant processes, such as apoptosis control, cell cycle regulation, or spindle formation. Others may represent novel cellular targets for the HPV oncogenes, such as a large group of C-MYC-associated genes involved in RNA splicing. Keywords: siRNA mediated knockdown
2007-07-01 | GSE6926 | GEO
Project description:Cornerstones of the regulatory phenomena observed in hypoxic HPV-positive cancer cells are: (i) hypoxia blocks E6/E7, an effect that can be counteracted by (ii) AKT inhibition and by (iii) high glucose supply. To gain further insights into the underlying regulatory circuits, mass spectrometry-based quantitative proteome analyses were performed comparing normoxic and hypoxic SiHa cells and assessing their response towards AKTi VIII and 25 mM glucose under hypoxia
2019-02-18 | PXD011095 | Pride
Project description:Aberrant glycosylation is a characteristic of tumor cells. The expression of certain glycan structures has been associated with poor prognosis. In cervical carcinoma has been reported changes in the gene expression level of some glycogenes that has been associated with lymph invasion. Human papilloma virus (HPV) infection is one of the most important factors to develop cervical cancer. HPV oncoproteins E6 and E7 have been implicated in cervical carcinogenesis. The role of these oncoproteins in glycosylation changes has not been reported. To know the effect of these oncoproteins on glycogene expression we realized a partial silencing of oncogenes E6 and E7 in HeLa cells, we made a microarray expression assay and we identified glycogenes that modified its expression. The analysis showed alteration in some glycosylation pathways, like glycosphingolipid, O-glycan mucin-type, and O-glycan non mucin-type glycosylation. Our results suggest that E6 and E7 oncoproteins could modified glycosylation of structures implicated in proliferation, adhesion, and apoptosis.
2016-12-07 | GSE90930 | GEO
Project description:The high-risk subgroup of Human papilloma viruses (HPVs), exemplified by HPV16/18, are causally linked to human cancers of the anogenital tract, skin, and upper aerodigestive tract. The high-risk HPV oncoproteins E6 and E7 are expressed from a polycistronic transcript that can potentially give rise to alternatively spliced E6 mRNAs, a process important for E6 and E7 expression and oncogenic transformation. Previously, we identified ECD, the human homologue of the Drosophila ecdysoneless gene, as a novel HPV16 E6-interacting protein using Yeast two-hybrid system. Here, we show that the C-terminal region of ECD selectively binds to high-risk but not to low-risk HPV E6 proteins. We demonstrate that ECD is overexpressed in HPV+ as well as HPV- cervical and head and neck patient tumor samples. Using the TCGA dataset, we show that ECD mRNA overexpression predicts shorter survival in these cancer patients. Recent work from our laboratory showed that ECD associates with several components of RNA biogenesis/splicing machinery and are involved in mRNA export. Here, we show that ECD is an RNA binding protein and regulates mRNA splicing. RNAseq analyses of SiHa cells upon ECD knockdown (KD) revealed alterations of many cellular pathways with prominent downregulation of components of the mRNA splicing machinery. Further investigation revealed that ECD KD resulted in dysregulation of E6 RNA splicing, resulting in decreased E7 and increased RB protein. Furthermore, ECD KD dysregulated several cellular mRNAs known to be critical for HPV oncogenesis. Finally, we demonstrate that while ECD KD in cervical cancer cell lines led to a reduction in oncogenic traits, ECD overexpression together with E7 led to the immortalization of keratinocytes. Taken together, our results support a novel role of ECD in transcription and in viral and cellular mRNA splicing to support HPV-driven oncogenesis.
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Project description:The human papillomavirus virus (HPV) is a proven cause of most human cervical cancers, and might have a role in other malignancies including vulva, skin, oesophagus, head and neck cancer. HPV has also been speculated to have a role in the pathogenesis of lung cancer. To validate the hypothesis of HPV involvement in small cell lung cancer pathogenesis we performed gene expression profile of transgenic mouse model of SCLC induced by HPV-16 E6/E7 oncoproteins. Gene expression profile of SCLC has been performed using Agilent whole mouse genome (4x44k) representing ~ 41000 genes and mouse transcripts. Samples were obtained from two HPV16-E6/E7 transgenic mouse model and from littermateM-bM-^@M-^Ys normal lung.
2014-05-27 | E-GEOD-23962 | biostudies-arrayexpress