HPV_Keratinocytes
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR894493_1.fastq.gz | Fastqsanger.gz | |||
| ERR894493_2.fastq.gz | Fastqsanger.gz | |||
| ERR894494_1.fastq.gz | Fastqsanger.gz | |||
| ERR894494_2.fastq.gz | Fastqsanger.gz | |||
| ERR894495_1.fastq.gz | Fastqsanger.gz |
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Project description:Human papillomavirus (HPV) induced immortalization of human foreskin keratinocytes (HFK) is a two-step process, including 1) the bypass of replicative senescence and acquisition of an extended lifespan, and 2) the outgrowth of immortal cells. Our previous study showed that the immortalization capacity of HPV is type dependent, as reflected by the presence or absence of a crisis period before reaching immortality. In the present study we determined how the HPV-type specific immortalization capacity relates to DNA damage induction and overall genomic instability. Early passage HFKs transduced with HPV types 16, 18, 31, 33, 35, 45, 51, 59, 66 and 70 showed an increased number of double strand DNA breaks compared to controls, without significant differences between the various HPV-types. However, immortal descendants of HPV-transduced HFKs that underwent a crisis period (HPV45-, 51-, 59-, 66- and 70-transduced HFKs) showed significantly more chromosomal aberrations compared to those without a crisis period (HPV16-, 18-, 31-, and 35-transduced HFKs) (p<0.01). In particular, regions on chromosome 5p, 8, and 9q were significantly more frequently altered in cells with crisis. Interestingly, the hTERT locus at 5p was exclusively gained in cell lines with crisis. Chromothripsis was detected in one of the HPV16-immortalized cell lines in which multiple rearrangements within chromosome 8 resulted in a gain of c-MYC. In conclusion, the present study shows that upon HPV-induced immortalization, the number of chromosomal aberrations is inversely related to the immortalization capacity of the virus type. This suggests that hrHPV types with reduced immortalization capacity in vitro, as reflected by a crisis period, require more genetic host cell aberrations to trigger immortalization. DNA copy number analysis of human keratinocytes transformed by high-risk HPV
2016-08-01 | E-GEOD-72063 | biostudies-arrayexpress
Project description:Human papillomavirus (HPV) induced immortalization of human foreskin keratinocytes (HFK) is a two-step process, including 1) the bypass of replicative senescence and acquisition of an extended lifespan, and 2) the outgrowth of immortal cells. Our previous study showed that the immortalization capacity of HPV is type dependent, as reflected by the presence or absence of a crisis period before reaching immortality. In the present study we determined how the HPV-type specific immortalization capacity relates to DNA damage induction and overall genomic instability. Early passage HFKs transduced with HPV types 16, 18, 31, 33, 35, 45, 51, 59, 66 and 70 showed an increased number of double strand DNA breaks compared to controls, without significant differences between the various HPV-types. However, immortal descendants of HPV-transduced HFKs that underwent a crisis period (HPV45-, 51-, 59-, 66- and 70-transduced HFKs) showed significantly more chromosomal aberrations compared to those without a crisis period (HPV16-, 18-, 31-, and 35-transduced HFKs) (p<0.01). In particular, regions on chromosome 5p, 8, and 9q were significantly more frequently altered in cells with crisis. Interestingly, the hTERT locus at 5p was exclusively gained in cell lines with crisis. Chromothripsis was detected in one of the HPV16-immortalized cell lines in which multiple rearrangements within chromosome 8 resulted in a gain of c-MYC. In conclusion, the present study shows that upon HPV-induced immortalization, the number of chromosomal aberrations is inversely related to the immortalization capacity of the virus type. This suggests that hrHPV types with reduced immortalization capacity in vitro, as reflected by a crisis period, require more genetic host cell aberrations to trigger immortalization.
2016-08-01 | GSE72063 | 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. 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:Acute expression of E7 oncogene from HPV-16 or HPV-18 is sufficient to overcome tumor necrosis factor-alfa (TNF) cytostatic effect on primary human keratinocytes. In the present study we investigated the molecular basis of E7-induced TNF resistance through a comparative analysis of the effect of this cytokine on the proliferation and global gene expression of organotypic cultures of normal and E7(wild type or mutant)-expressing keratinocytes.
2010-01-15 | GSE17892 | GEO
Project description:Global long non-coding RNA (lncRNA) expression profile in primary human keratinocytes post-expression of high-risk HPV-16 E6 oncoprotein Purpose: The goal of this study is to utlize high-throughput RNA sequencing (RNA-seq) to identify differentially expressed host lncRNAs with the presence of the high-risk HPV-16 E6 oncoprotein in primary human foreskin keratinocytes. Methods: Primary human foreskin keratinocytes (HEKa) stably expressing HPV-16 E6 compared to GFP control were analyzed, in triplicates, by RNA-seq (Illumina). qRT-PCR validation was performed using SYBR Green assays. Results: 151 up- and 100 down-regulated host lncRNAs were altered greater than 1.5-fold change in HEKa expressing HPV-16 E6 compared to GFP control cells. Altered expression of 16 genes (8 up- and 8 down-regulated) were confirmed by qRT-PCR, demonstrating the high-degree of sensitivity of the RNA-seq method. Conclusions: Our study represents the first global screening of host lncRNAs altered specifically by HPV-16 E6 oncoprotein expression.
2018-10-31 | GSE115334 | GEO
Project description:Acute expression of E7 oncogene from HPV-16 or HPV-18 is sufficient to overcome tumor necrosis factor-alfa (TNF) cytostatic effect on primary human keratinocytes. In the present study we investigated the molecular basis of E7-induced TNF resistance through a comparative analysis of the effect of this cytokine on the proliferation and global gene expression of organotypic cultures of normal and E7(wild type or mutant)-expressing keratinocytes. In order to determine the effects of E7 expression on TNF response, we performed 3 independent experiment for each cell line. Organotypic cultures of normal and E7(wild type or mutant)-expressing keratinocytes were treated with 2 nM TNF for 72 hours, or left untreated.
2010-06-24 | E-GEOD-17892 | biostudies-arrayexpress
Project description:Human papillomaviruses (HPV) preferentially infect keratinocytes of mucous membranes or skin and cause numerous benign and malignant lesions at different anatomical locations. We sequenced small RNA (sRNA) libraries of two HPV 16 immortalized cell lines and ten formalin fixed paraffin embedded (FFPE) tissue samples from HPV infected cervical epithelium by SOLiD 4 technology.
2020-06-30 | GSE62239 | GEO
Project description:HPV alters the host transcriptional program to establish infection and complete its lifecycle. Infection of keratinocytes has been difficult until our development of extracellular matrix (ECM) to cell transfer system that allows efficient infection of primary keratinocytes. Using this model, the transcriptional program of HPV infected keratinocytes at different times post infection was analyzed by mRNA-seq.
2019-11-10 | GSE137361 | GEO
Project description:HPV alters the host transcriptional program to establish infection and complete its lifecycle. Infection of keratinocytes has been difficult until our development of extracellular matrix (ECM) to cell transfer system that allows efficient infection of primary keratinocytes. Using this model, the transcriptional program of HPV infected keratinocytes grown in raft culture was analyzed by mRNA-seq.
2019-11-10 | GSE137964 | GEO
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