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Transgenic SCLC induced by E6/E7 oncoproteins vs normal controls

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE23962 | GEO | 2014/05/27

SECONDARY ACCESSION(S): PRJNA130389

REPOSITORIES: GEO

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Transgenic SCLC induced by E6/E7 oncoproteins vs normal controls

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

Effect of HPV 16 E6, E7 oncoproteins on the expression level of cellular genes

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

Effect of HPV 16 E6, E7 oncoproteins on the expression level of cellular genes

2014-06-26 | GSE58841 | GEO

Identification of downstream targets of the human papillomavirus E6 and E7 oncoproteins by RNA interference

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

Identification of host transcriptional networks showing concentration-dependent regulation by HPV16 E6 and E7 proteins in basal cervical squamous epithelial cells.

Project description:The W12 cell lineage recapitulates the early events in HPV-driven cervical cancer pathogenesis (which is impossible to investigate using clinical samples) and we are interested in characterising the host transcriptional events that occur at those early stages. Previous work in these cells has identified early biomarkers of cervical cancer (now in widespread commercial use) as well as critical pathways in cervical carcinogenesis. By taking a network-based approach to the whole transcriptome we have identified important master regulators of a tightly and quantitatively regulated expression response to HPV early gene expression. Briefly, transcriptional activity of 16 different clones form the W12 cell line were measured in parallel. Each clone has measured HPV early gene activity at mRNA and protein level, as well as cell growth rates as previously described in Scarpini et al 2014 J Pathol July; 233(3): 281â293 (PubmedID 24752734; DOI: 10.1002/path.4358; http://europepmc.org/articles/PMC4285939#b11).

2016-11-30 | E-MTAB-4409 | biostudies-arrayexpress

E6^E7, a novel splice isoform protein of human papillomavirus 16, stabilizes viral E6 and E7 oncoproteins via HSP90 and GRP78.

Project description: Not available

| S-EPMC4337564 | biostudies-literature

Comparative analysis of mouse oropharyngeal cells expressing HPV16 E6/E7, hRas, and luciferase (mEERL) with mEERL lung metastasis cell lines (MLM)

Project description:Human papillomavirus (HPV) is currently the most identifiable cause of head and neck squamous cell carcinoma (HNSCC) accounting for approximately 25% of these cases. HPV+ cancer incidence is on the rise with metastatic disease accounting for nearly all HPV+ HNSCC related deaths. Thus, developing a relevant in vivo pre-clinical model for these invasive cancers is necessary for testing new disease therapeutics and improving survival. To this end, we characterize a novel metastatic HPV+ murine model of HNSCC. Individual metastatic clonal cell lines were isolated from an animal with late pulmonary metastasis that developed recurrent disease after standard of care cisplatin-radiation therapy. Similar to the parental cells, all metastatic cell lines retain expression of HPV16 E6 and E7 oncogenes and degrade P53. While the in vitro growth rates of these metastatic clones are slower than the parental tumor line their in vivo growth is greatly enhanced. Moreover, resistance to standard therapies (cisplatin and radiation) is dramatically increased in 3 of the 4 clones in vivo. Lymphatic and/or lung metastasis occurs 100% of the time in 2 of the clonal lines while it is nearly undetectable in the parental line. In addition, expression and protein array analyses were completed to investigate the mechanisms driving these phenotypic changes. This model not only provides an economical and rapid screening system in which to develop and test improved therapeutic regimens but may also provide mechanistic insights into tumor metastasis.

2016-04-15 | GSE68935 | GEO

Docosahexaenoic acid induces the degradation of HPV E6/E7 oncoproteins by activating the ubiquitin-proteasome system.

Project description: Not available

| S-EPMC4260735 | biostudies-literature

Intrabodies targeting human papillomavirus 16 E6 and E7 oncoproteins for therapy of established HPV-associated tumors.

Project description: Not available

| S-EPMC7825221 | biostudies-literature

Impact of HPV16 E6 and E7 oncogenes together with Chlamydia trachomatis infection on proteome changes in immortalized oral keratinocytes

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

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