Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA94785 | ENA |
REPOSITORIES: ENA
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Project description:Integration of high-risk human papillomavirus (HRHPV) into the host genome is a key event in cervical neoplastic progression. Integration is associated with deregulated expression of the viral oncogenes E6 and E7 and acquisition of a selective growth advantage for cells containing integrants. Overexpression of the viral transcriptional regulator E2 from heterologous promoters has an inhibitory effect on transcription from integrated HRHPV. We therefore hypothesised that loss of E2-expressing episomes from cells in which integration had previously occurred would be required for such cells to gain a growth advantage. Using the unique W12 model of cervical squamous carcinogenesis, we show that cells containing integrated HPV16 reproducibly emerged during long-term culture when there had been a rapid fall in episome numbers. During the period of emergence it is possible to isolate single-cell clones containing an intracellular mixture of the integrant being selected and episomes at reduced load. Microarray analysis showed that episome loss was closely associated with endogenous activation of antiviral response genes that are also inducible by the type I interferon (IFN) pathway. Taken together, our results indicate that episome loss, associated with induction of antiviral response genes, is a key event in the spontaneous selection of cervical keratinocytes containing integrated HPV16. We conclude that cervical carcinogenesis requires not only HRHPV integration, but also loss of inhibitory episomes. Keywords: Time course, human papillomavirus, episome loss
2006-02-24 | GSE4289 | GEO
Project description:To investigate the extent of host methylome dysregulation by the human papillomavirus (HPV) oncoprotein E7, we performed methylome array analysis on normal immortalized keratinocytes from skin (NIKS), NIKS cells maintaining the HPV16 or 18 episomes (NIKS-16, NIKS-18, respectively), and NIKS cells maintaining the HPV-16 episome deficient in E7 expression (NIKS-16ΔE7).
2017-06-11 | GSE83261 | GEO
Project description:W12 clones, naturally infected with HPV16, were passaged under non-competitive conditions until the virus had integrated and they were episome free. RNA-seq was performed in duplicate for 5 W12 clone lines, normal cervix tissue and a parental W12 line.
2021-06-18 | E-MTAB-10155 | biostudies-arrayexpress
Project description:To investigate the extent of gene expression dysregulation by the human papillomavirus (HPV) oncoprotein E7, we performed global gene expression analysis on normal immortalized keratinocytes from skin (NIKS), NIKS cells maintaining the HPV16 or 18 episomes (NIKS-16, NIKS-18, respectively), and NIKS cells maintaining the HPV-16 episome deficient in E7 expression (NIKS-16ΔE7).
2017-06-11 | GSE83259 | GEO
Project description:We utilised our in vitro model of cervical neoplastic progression, W12, to investigate the effect of HPV16 viral oncogene depletion on well-defined integrant- and episome- associated series. To target HPV16 viral oncogenes we used our previously published E7-targeting siRNA sequence that caused substantial depletion of both E7 and E6 in CaSki cells. We found all E7-siRNA treated W12 series underwent widespread autophagy and senescence, with up-regulation of an innate immune response.
2013-08-12 | E-MTAB-1331 | biostudies-arrayexpress
Project description:Certain types of Human papilloma viruses (HPV) are the etiological agents for cervical cancer. However, not all infections of high-risk HPVs will finally lead to cancer since most HPV infections are cleared without any consequences. Chlamydia trachomatis is the most prevalent sexual transmitted bacteria and is an obligatory intracellular pathogen exhibiting tropism in endocervical epithelial cells. Over the past decades, C. trachomatis is thought to be a potential co-factor for cervical cancer formation, but there are also studies that did not show such a correlation. To address this question in molecular terms, we stably expressed HPV16 E6 and E7 in spontaneously immortalized NOKs (normal oral keratinocytes) and performed SILAC (stable isotope labeling by amino acids in cell culture) with or without C. trachomatis infection to study the impact of HPV16 oncogene expression and C. trachomatis infection on host proteome changes.
2019-03-18 | PXD012186 | Pride
Project description:We used freshly established immortalized human keratinocytes with a well-defined HPV16 E6 E7 expression cassette to get a more complete and less biased overview about global changes induced by HPV16 using RNA-seq. We identified novel factors regulated by HPV oncogenes that could serve an essential role in cancer development.
2019-03-03 | GSE124357 | 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 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
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:Previous studies have shown that normal and HPV immortalized keratinocytes are sensitive to TNF anti-proliferative effect. Conversely, HPV18-immortalized keratinocytes are resistant to the cytostatic effect mediated by this cytokine. In this study we have compared gene expression patterns in primary cultures of human foreskin epidermal keratinocytes (PHK or NHFK) and HPV16 (HF698) and HPV18(HF18Nco)-immortalized cell lines, and profile the transcriptional changes 3 and 60 hours after TNF treatment. Keywords: global expression profile, microarray, HPV, TNF In order to determine the effects of HPV infection and TNF treatment on global gene expression, were performed 2 independent experiment for each cell line, including the two periods of treatment with TNF. Furthermore, were performed 2 experiments for each control plate containing the non-treated cells.
2007-08-25 | E-GEOD-4524 | biostudies-arrayexpress