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Differential gene expression between skin and cervix induced by the E7 oncoprotein in a transgenic mouse model

ABSTRACT: HPV16 E7 oncoprotein expression in K14E7 transgenic mice induces cervical cancer after 6 months of treatment with the co-carcinogen 17β-estradiol. In untreated mice, E7 also induces skin tumors late in life, albeit at low penetrance. These findings indicate that E7 alters cellular functions in cervix and skin so as to predispose these organs to tumorigenesis. Using microarrays, we determined the global genes expression profile in cervical and skin tissue of young adult K14E7 transgenic mice without estrogen treatment. In these tissues, the E7 oncoprotein altered the transcriptional pattern of genes involved in several biological processes, including immune response, intracellular signaling cascades, cell adhesion, cell migration, development, cell cycle, growth, response to wounding and regulation of apoptosis. Among the E7-dysregulated genes were ones not previously known to be involved in cervical neoplasia, including DMBT1, GLI1 and 17βHSD2 in cervix and MMP2, 12, 14, 19 and 27 in skin.

ORGANISM(S): Mus musculus

PROVIDER: GSE36219 | GEO | 2012/06/10

SECONDARY ACCESSION(S): PRJNA153121

REPOSITORIES: GEO

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Differential gene expression between skin and cervix induced by the E7 oncoprotein in a transgenic mouse model

Project description:HPV16 E7 oncoprotein expression in K14E7 transgenic mice induces cervical cancer after 6 months of treatment with the co-carcinogen 17M-NM-2-estradiol. In untreated mice, E7 also induces skin tumors late in life, albeit at low penetrance. These findings indicate that E7 alters cellular functions in cervix and skin so as to predispose these organs to tumorigenesis. Using microarrays, we determined the global genes expression profile in cervical and skin tissue of young adult K14E7 transgenic mice without estrogen treatment. In these tissues, the E7 oncoprotein altered the transcriptional pattern of genes involved in several biological processes, including immune response, intracellular signaling cascades, cell adhesion, cell migration, development, cell cycle, growth, response to wounding and regulation of apoptosis. Among the E7-dysregulated genes were ones not previously known to be involved in cervical neoplasia, including DMBT1, GLI1 and 17M-NM-2HSD2 in cervix and MMP2, 12, 14, 19 and 27 in skin. The experiment consists of a total of 24 samples to evaluate the mRNA expression profiles in 4 different groups: skin biopsy of transgenic mice K14E7, cervix biopsy of transgenic mice K14E7, skin biopsy of FVB/N control virgin mice and cervix biopsy of FVB/N control virgin mice. Each group has 6 samples that had been processed in 3 pools of two samples (biological replicates) for a total of 6 samples for each condition.

2012-06-09 | E-GEOD-36219 | biostudies-arrayexpress

GENE EXPRESSION PROFILE REGULATED BY THE HPV16-E7 ONCOPROTEIN AND ESTRADIOL IN CERVICAL TISSUE

Project description:The HPV16-E7 oncoprotein and 17Î²-estradiol are import factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. In this study, we performed a microarray analysis to obtain a global gene expression profile induced by both, HPV16-E7 and 17Î²-estradiol in cervical tissue of K14E7 transgenic mice. We found that 17Î²-estradiol is the main cause of the up-regulation of a large number of cellular genes involved in the immune response whereas E7 oncoprotein mainly affects the cellular metabolism. Our microarray data also shows some novel differentially expressed genes that were not previously reported in cervical cancer. The identification of these genes, regulated by E7 and 17Î²-estradiol, provides the basis for further studies on their role in cervical carcinogenesis. 15 Mouse Gene 1.0 ST Affymetrix microarrays were used to analyze gene expression of cervical tissue from K14E7 hemizygote and nontransgenic FvB control virgin female untreated and treated mice. Briefly, one-month virgin female transgenic and nontransgenic mice were implanted in the dorsal skin with continuous release pellets delivering 0.05 mg of17-Î² estradiol over 60 days. As control samples we used K14E7 and FvB untreated mice. For the microarray analysis we used triplicates for each group (3 treated K14E7 mice, 3 treated FvB mice, 3 untreated K14E7 mice, 3 untreated FvB mice).

2013-07-01 | E-GEOD-46890 | biostudies-arrayexpress

GENE EXPRESSION PROFILE REGULATED BY THE HPV16-E7 ONCOPROTEIN AND ESTRADIOL IN CERVICAL TISSUE

Project description:The HPV16-E7 oncoprotein and 17β-estradiol are import factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. In this study, we performed a microarray analysis to obtain a global gene expression profile induced by both, HPV16-E7 and 17β-estradiol in cervical tissue of K14E7 transgenic mice. We found that 17β-estradiol is the main cause of the up-regulation of a large number of cellular genes involved in the immune response whereas E7 oncoprotein mainly affects the cellular metabolism. Our microarray data also shows some novel differentially expressed genes that were not previously reported in cervical cancer. The identification of these genes, regulated by E7 and 17β-estradiol, provides the basis for further studies on their role in cervical carcinogenesis.

2013-07-01 | GSE46890 | GEO

Effect of HPV8-E7 expression on the secretome of keratinocytes

Project description:Human papillomavirus type 8 (HPV8) is associated with the development of non-melanoma skin cancer. In the past we already delved into the mechanisms involved in keratinocyte invasion, showing that the viral E7 oncoprotein is a key player that drives invasion of basal keratinocytes controlled by the extracellular protein fibronectin. To unravel further downstream effects in E7 expressing keratinocytes we now characterized alterations of the secretome of E7 expressing N/TERT keratinocytes.

2022-02-17 | PXD026100 | Pride

Effect of HPV8-E7 expression on the phospho-proteome in keratinocytes

2022-02-17 | PXD026099 | Pride

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

High-risk human papillomavirus E7 affects host keratinocyte DNA methylation

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

High-risk human papillomavirus E7 affects host keratinocyte gene expression

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

E5 human papillomavirus type 16 oncoprotein modify ST3GAL3 and ST6GAL1 gene expression

Project description:Human papillomavirus (HPV) is the etiological agent of cervical cancer. Three viral proteins, E5, E6 and E7 have been implicated in cell transformation. Increased expression of sialic acid and sialylated antigens have been reported during cervix transformation, these results agree with the increased mRNA levels of the sialyltransferases genes ST6GAL1 and ST3GAL3 reported in premalignant and malignant tissue of the cervix. E6 and E7 HPV oncoproteins modify the expression of some glycogenes. The role of E5 HPV oncoprotein in the glycogene expression changes in premalignant and malignant cervical tissue has not been reported. The objective of this work was to identify glycogenes that modify their expression by E5 HPV oncoprotein in HaCaT cell line. A gene expression microarray was performed on HaCaT cells that stably expressed the HPV16 E5 oncogene. Analysis revealed alteration in some glycogenes including upregulation of ST6GAL1 and ST3GAL3. The increased mRNA levels of both genes were confirmed by qRT-PCR. In addition, an in-silico analysis was performed to identify glycosylation networks altered in presence of E5 oncoprotein. The analysis showed that E5 could modify the sialic acid expression, keratan sulfate synthesis, N-glycosylation and biosynthesis of glycosaminoglycans. This is the first report of the role of HPV16 E5 oncoprotein on glycogenes expression changes. Moreover, our results suggest that the increase of the sialyltransferases genes reported in premalignant and malignant cervical tissue, could be the result of the expression of E5 oncoprotein. These results provide information of the possible role of HPV infection on the sialylation changes in the cervical epithelium identified in premalignant lesions and cancer.

2018-08-21 | GSE118776 | GEO

Transgenic SCLC induced by E6/E7 oncoproteins vs normal controls

2014-05-27 | GSE23962 | GEO

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