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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human cervical keratinocytes infected with HPV16

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

DISEASE(S): integrated HPV16 only

SUBMITTER: Mark Robert Pett

PROVIDER: E-GEOD-4289 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Selection of cervical keratinocytes containing integrated HPV16 associates with episome loss and an endogenous antiviral response.

Pett Mark R MR Herdman M Trent MT Palmer Roger D RD Yeo Giles S H GS Shivji Mahmud K MK Stanley Margaret A MA Coleman Nicholas N

Proceedings of the National Academy of Sciences of the United States of America 20060227 10

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. Therefore, we hypothesized that loss of E2-expressing ep ...[more]

PMID: 16505361

Similar Datasets

Host transcriptome changes associated with episome loss and selection of keratinocytes containing integrated HPV16

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

Expression signatures and cytogenetic aberrations in HPV16 E6, E7 and E6/E7-positive immortalized human epithelial cells

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

Human HPV16 positive CaSki cells: Control vs. virus oncogene e6/e7 silenced

Project description:The infection with high-risk human papillomavirus is aetiologically linked to cervical cancer, the role of miRNAs regulated by virus oncogene in cancer progression remain largely unknown. Here, we screened the differentially expressed miRNAs with miRNA array between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines In the study, we screened the differentially expressed miRNAs with miRNA array (Exiqon, miRCURY LNA microRNA array, 7th gen [hsa, miRBase 18]) between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines to found miRNAs regulated by virus oncogene e6/e7. Biological replicates: 3 control, 3 e6/e7 silenced, independently grown and harvested. four replicates per array.

2016-07-01 | E-GEOD-68153 | biostudies-arrayexpress

Human Papillomavirus (HPV) genomic integration, expression and E6/E7 splicing patterns in cervical cancer associated with HPV16 or HPV18 infection

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

High risk HPV-positive lung carcinomas: molecular evidence for a pattern of pulmonary metastasis

Project description:BACKGROUND: Infection with high-risk types of human papillomavirus (hrHPV) is associated with cervical, anogenital and oropharyngeal cancers. A role for hrHPV in lung cancer has been proposed, although previous reports on the contribution of hrHPV infection to lung cancer have provided contradictory results. The current study evaluated hrHPV prevalence in lung tumor specimens of different histological subtypes in a Western study population using a validated test algorithm for hrHPV detection in formalin-fixed paraffin-embedded (FFPE) tumor specimen (i.e., GP5+6+-PCR and p16INK4A immunohistochemistry). MATERIALS AND METHODS: Tumor tissue specimens from 228 lung cancer patients were subjected to GP5+6+-PCR and p16INK4A immunohistochemistry. hrHPV-positive tumors were further characterized using genotyping of GP5+/6+-PCR products, HPV E7 transcript analysis, loss of heterozygosity (LOH) analysis and array comparative genomic hybridization (arrayCGH), and the clinical history of patients was retrieved. RESULTS: Three patients (3/228, 1.3%) with hrHPV-positive lung tumors were identified, revealing hrHPV types 16, 18 and 33, respectively. All three patients (1 male, 2 females) had a history of hrHPV-associated disease; two cervical carcinoma, and one oropharyngeal carcinoma. Further characterization revealed identical hrHPV genotype, pattern of p16INK4A expression, HPV E7 mRNA expression, and genomic aberrations in the individual pairings of lung tumor and foregoing hrHPV-associated cancer. CONCLUSION: The present study found molecular evidence that supports association of hrHPV in lung cancer with the presence of pulmonary metastasis of a hrHPV-positive cancer that originated elsewhere, and not with primary lung cancer in a Western population. 2 lung cancer samples (FFPE), 1 cervical cancer sample (FFPE), 1 head and neck cancer sample (FFPE)

2013-07-01 | E-GEOD-40777 | biostudies-arrayexpress

Human HPV16 positive CaSki cells: Control vs. virus oncogene e6/e7 silenced

2016-07-01 | GSE68153 | GEO

Transcription profiling of human head and neck squamous cell carcinoma samples reveals a feed-forward loop involving protein kinase Calpha and microRNAs regulates tumor cell cycle

Project description:Patient selection and specimen collection. Thirty-six freshly frozen tumor samples were prospectively collected from patients undergoing surgery or biopsy for HNSCC at the University of North Carolina (UNC) at Chapel Hill (21 patients) and Vanderbilt University (15 patients). All tissues were snap-frozen in liquid nitrogen within 30 minutes of surgical resection or biopsy, and kept at -80oC until further processing. All patients consented to participation in this study under protocols approved by IRB at the two institutions. This set includes the samples previously deposited into GEO including 8 additional samples and adjustment for protocol changes. The original 36 before protocol changes (and thus unadjusted) are here: Slebos RJ, Yi Y, Ely K, et al. Gene expression differences associated with human papillomavirus status in head and neck squamous cell carcinoma. Clin Cancer Res 2006;12(3 Pt 1):701-9. Experiment Overall Design: 44 primary head and neck tumor samples

2009-03-28 | E-GEOD-10300 | biostudies-arrayexpress

MicroRNA expression profile in human foreskin keratinocytes (HFKs) transduced with retroviral vectors carrying E6 and E7 genes of either HPV6 or HPV16 and with the LXSN empty vector

Project description:Cervical cancer is a leading cause of cancer-related death in women worldwide. Nearly all cases of cervical cancer are attributed to infection with human papillomavirus (HPV), mainly high-risk type HPV16 and HPV18. Two viral genes, E6 and E7, play an important role in viral life cycle, since they delay keratinocyte differentiation and stimulate cell cycle progression, allowing the virus to exploit host DNA replication machinery to replicate its genome. Some of the oncogenic properties of E6 and E7 are mediated by host microRNAs (miRNAs) involved in the control of cell proliferation, senescence, and apoptosis. In order to identify genome-wide changes in miRNA expression profile, miRNA microarray analysis was performed on HFKs transduced with retroviral vectors carrying E6 and E7 genes of either HPV6 or HPV16 and with the LXSN empty vector. This dataset was used to identify and to further investigate the role of miR-146a-5p in cervical cancer.

2018-01-16 | E-MTAB-6360 | biostudies-arrayexpress

High risk HPV-positive lung carcinomas: molecular evidence for a pattern of pulmonary metastasis

2013-07-01 | GSE40777 | GEO

Gene expression analysis of laser-captured epithelium and stroma from FVB mice and HPV16 E6/E7 transgenic mice under estrogen or control treatment regimens.

Project description:Affymetrix Mouse Genome 430 2.0 arrays were used to measure genome-wide gene expression levels. The results show that high-risk human papillomavirus oncogenes E6 and E7 reprogram the cervical cancer microenvironment independently of and synergistically with estrogen, a critical co-factor in cervical cancer development and maintenance. Several potential estrogen-induced paracrine-acting factors were identified in the expression profile of the cervical tumor microenvironment. The microenvironment of estrogen-treated HPV-transgenic mice was significantly enriched for chemokine/cytokine activity and inflammatory and immune functions associated with carcinogenesis.

2018-01-09 | GSE102232 | GEO

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