Tissue-specific gene expression during productive HPV16 infection of cervical, foreskin and tonsil epithelium.
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ABSTRACT:
PROVIDER: PRJNA530248 | ENA |
REPOSITORIES: ENA
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Project description:We performed microarray analysis of the effect of productive HPV16 infection in cervical, foreskin and tonsil epithelial trancriptome. Our study for the first time compares and contrast the gene expression changes and differential activation of cellular pathways induced by the virus in the three tissue types.
2019-06-03 | GSE129159 | GEO
Project description:Microarray analysis of the effect of early stage, productive HPV16 infection on the transcriptome of human cervical keratinocytes. Our results provide for the first time, global gene expression changes in cervical epithelium that produces high levels of viral titers.
2018-07-24 | GSE109039 | GEO
Project description:The effect of productive HPV16 infection on the cervical epithelium transcriptome
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Project description:To explore the circRNA expression profiles during the development and progression of cervical cancer, we performed RNA sequencing analysis with ribosomal RNA-depleted in HPV negative normal cervical epithelium, HPV16 positive normal cervical epithelium, HPV16 positive high-grade squamous intraepithelial lesion (HSIL), and HPV16 positive cervical squamous cell carcinoma tissues,6 cases in each group.Totally 66868 circRNAs were identified (Back-spliced junctions reads≥1)
2020-12-21 | GSE147009 | GEO
Project description:CircRNAs have been found to regulate mRNA expression levels and serve an important role in cervix carcinogenesis. To explore the circRNA expression profiles during the development and progression of cervical cancer, we performed microarray analysis with total RNA in normal cervical epithelium(n=7), HPV16 positive high-grade squamous intraepithelial lesion (HSIL)(n=6), and HPV16 positive cervical squamous cell carcinoma tissues(n=7).
2021-02-10 | GSE166466 | GEO
Project description:This RNA-seq study in primary human forekin keratinocytes was to define genes that are differetially expressed in the presence or absence of HPV16 E7 or several HPV16 E7 variants. We also generated and conducted RNA-seq on primary human foreskin keratinocytes that were CRISPR-Cas9 edited with nontargeting sgRNA or sgRNA targeting PTPN14.
2019-02-28 | GSE121906 | GEO
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
Project description:Epidemiological data confirm a much higher incidence of high-risk human papillomavirus 16 (HPV16)-mediated carcinogenesis of the cervical epithelium than for other target sites. In order to elucidate tissue-specific responses to virus infection, we compared gene expression changes induced by productive HPV16 infection of cervical, foreskin, and tonsil organotypic rafts. These rafts closely mimic persistent HPV16 infection, long before carcinogenesis sets in. The total number of gene expression changes varied considerably across the tissue types, with only 32 genes being regulated in common. Among them, we confirmed the Kelch-like family protein KLHL35 and the laminin-5 complex to be upregulated and downregulated, respectively, in all the three tissues. HPV16 infection induces upregulation of genes involved in cell cycle control, cell division, mitosis, DNA replication, and DNA damage repair in all the three tissues, indicative of a hyperproliferative environment. In the cervical and tonsil epithelium, we observe significant downregulation of genes involved in epidermis development, keratinocyte differentiation, and extracellular matrix organization. On the other hand, in HPV16-positive foreskin (HPV16 foreskin) tissue, several genes involved in interferon-mediated innate immunity, cytokine signaling, and cellular defenses were downregulated. Furthermore, pathway analysis and experimental validations identified important cellular pathways like STAT1 and transforming growth factor β (TGF-β) to be differentially regulated among the three tissue types. The differential modulation of important cellular pathways like TGF-β1 and STAT1 can explain the sensitivity of tissues to HPV cancer progression.IMPORTANCE Although the high-risk human papillomavirus 16 infects anogenital and oropharyngeal sites, the cervical epithelium has a unique vulnerability to progression of cancer. Host responses during persistent infection and preneoplastic stages can shape the outcome of cancer progression in a tissue-dependent manner. Our study for the first time reports differential regulation of critical cellular functions and signaling pathways during productive HPV16 infection of cervical, foreskin, and tonsil tissues. While the virus induces hyperproliferation in infected cells, it downregulates epithelial differentiation, epidermal development, and innate immune responses, according to the tissue type. Modulation of these biological functions can determine virus fitness and pathogenesis and illuminate key cellular mechanisms that the virus employs to establish persistence and finally initiate disease progression.
| S-EPMC6694821 | biostudies-literature
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. 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-β 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
Project description:Human papillomavirus (HPV) genome integration into the host genome, blocking E2 expression and leading to overexpression of E6 and E7 viral oncogenes, is considered a major step in cervical cancer development. In high-risk HPVs, E6 and E7 oncogenes are expressed as a bicistronic pre-mRNA, with alternative splicing producing the ultimate mRNAs required for E6 and E7 translation. Given the number of alternative donor and acceptor splicing sites, ten E6/E7 different alternative transcripts might be formed for HPV16 and three for HPV18, although only six isoforms have been previously reported for HPV16. In the present work, we employ high-throughput sequencing of invasive cervical cancer transcriptome (RNA-Seq) to characterize the expression of the HPV genome in 24 invasive cervical cancers associated with HPV16 and HPV18 single infections. Based on high-resolution transcriptional maps, we herein report three viral gene expression patterns which might be associated with the presence of the viral genome in episomal and/or integrated stages. Alternative mRNAs splicing isoforms coding for E6 and E7 oncoproteins were characterized and quantified, and two novel isoforms were identified. Three major isoforms (E6*I, E6*II, and E6+E7) were detected for HPV16 and two for HPV18 (E6*I and E6+E7). Minor transcript isoforms, including the novel ones, were very rare in some tumor samples or were not detected. Our data suggested that minor transcript isoforms of E6/E7 do not play a relevant role in cervical cancer.
2019-08-06 | GSE91065 | GEO