Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

26 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Angela Grassi

PROVIDER: E-MTAB-6360 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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

MicroRNA analysis in HPV-positive and HPV-negative cervical cancer cell lines

Project description:Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. MiRNA expression profile was investigated by microrray analysis in the HPV-positive cervical cancer cell lines SiHa (HPV16-positive cell line derived from a cervical squamous cell carcinoma), CaSki (HPV16-positive cell line derived from a metastatic cervical epidermoid carcinoma), and HeLa (HPV18-positive cell line derived from a cervical adenocarcinoma) and compared with primary HFKs and C33a (HPV-negative cervical cell line).

2018-01-16 | E-MTAB-6361 | biostudies-arrayexpress

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

2016-07-01 | GSE68153 | GEO

Effects of hypoxia on antigen presentation and T cell-based immune recognition of HPV16-transformed cells

Project description:Attempts to develop a therapeutic vaccine against human papillomavirus (HPV)-induced malignancies have not been clinically successful to date. One reason may be the hypoxic microenvironment present in most tumors, including cervical cancer. Hypoxia dysregulates the levels of human leukocyte antigen (HLA) class I molecules in different tumor entities, impacts function of cytotoxic T cells, and leads to decreased protein levels of the oncoproteins E6 and E7 in HPV-transformed cells. Therefore, we investigated the effect of hypoxia on the presentation of HPV16 E6- and E7-derived epitopes in cervical cancer cells and its effect on epitope-specific T cell cytotoxicity. Hypoxia induced downregulation of E7 protein levels in all analyzed cell lines, as assessed by Western blotting. However, contrary to previous reports, no perturbation of antigen presentation machinery (APM) components and HLA-A2 surface expression upon hypoxia treatment was detected by mass spectrometry and flow cytometry, respectively. Cytotoxicity assays performed in hypoxic conditions showed differential effects on the specific killing of HPV16-positive cervical cancer cells by epitope-specific CD8+ T cell lines in a donor- and peptide-specific manner. Effects of hypoxia on the expression of PD-L1 were ruled out by flow cytometry analysis. Altogether, our results suggest an intact APM, and cytotoxicity despite the decreased expression of E6 and E7, suggesting that successful immunotherapies can be developed for HPV-induced cervical cancer, especially if combined with hypoxia-alleviating measures.

2022-11-16 | PXD032217 | 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

Depletion of HPV16 oncogenes induces autophagy and senescence in a cervical carcinogenesis model, irrespective of viral physical state

Project description:We utilised our in vitro model of cervical neoplastic progression, W12, to investigate the effect of HPV16 viral oncogene depletion on well-defined integrant- and episome- associated series. To target HPV16 viral oncogenes we used our previously published E7-targeting siRNA sequence that caused substantial depletion of both E7 and E6 in CaSki cells. We found all E7-siRNA treated W12 series underwent widespread autophagy and senescence, with up-regulation of an innate immune response.

2013-08-12 | E-MTAB-1331 | biostudies-arrayexpress

Nuclear Lactate Dehydrogenase A Senses ROS to Produce α-Hydroxybutyrate for HPV-Induced Cervical Tumor Growth

Project description:It is well known that high-risk human papilloma virus (HR-HPV) infection is strongly associated with cervical cancer and E7 was identified as one of the key initiators in HPV-mediated carcinogenesis. Here we show that lactate dehydrogenase A (LDHA) preferably locates in the nucleus in HPV16-positive cervical tumors due to E7-induced intracellular reactive oxygen species (ROS) accumulation. Surprisingly, nuclear LDHA gains a non-canonical enzyme activity to produce α-hydroxybutyrate and triggers DOT1L (disruptor of telomeric silencing 1-like)-mediated histone H3K79 hypermethylation, resulting in the activation of antioxidant responses and Wnt signaling pathway. Furthermore, HPV16 E7 knocking-out reduces LDHA nuclear translocation and H3K79 tri-methylation in K14-HPV16 transgenic mouse model. HPV16 E7 level is significantly positively correlated with nuclear LDHA and H3K79 tri-methylation in cervical cancer. Collectively, our findings uncover a non-canonical enzyme activity of nuclear LDHA to epigenetically control cellular redox balance and cell proliferation facilitating HPV-induced cervical cancer development.

2018-09-24 | PXD011058 | Pride

RNA expression profile comparison of HFKs expressing E6/E7 from beta-3 HPVs (49, 75, 76, 115) and from HR alpha HPV16 and beta-2 HPV38

Project description:Comparative analysis of RNA expression profiles of keratinocytes expressing E6/E7 from the different beta-3, with the RNA profiles of HPV16 and HPV38 E6/E7 HFKs reveals that HPV115 is the more divergent from the HR-mucosal type. Moreover beta-3 HPV 49, 75 and 76 E6/E7 HFKs show altered expression of genes involved in cell cycle regulation and DNA damage response which are also deregulated by expression of E6/E7 of HPV16.

2020-07-04 | GSE100681 | GEO

Expression data from SIX1 knocked-down HKc/DR cells

Project description:The homeodomain transcription factor SIX1 plays a critical role in embryogenesis, is not expressed in normal adult tissue, but is expressed in many malignancies, including cervical cancer. SIX1 drives the progression of HPV16-immortalized human keratinocytes (HKc/HPV16) toward malignancy: HKc/HPV16 express high levels of SIX1 mRNA and protein; overexpression of SIX1 in HKc/HPV16 produces pre-malignant, differentiation-resistant lines (HKc/DR); SIX1 overexpression in HKc/DR induces tumorigenicity. In this paper, we explore the consequences of inhibition of SIX1 expression in premalignant HKc/DR. Only partial inhibition of SIX1 expression could be obtained in HKc/DR by RNA interference. Decreased SIX1 expression (up to 80%) in HKc/DR resulted in slower proliferation, decreased HPV16-E6/E7 mRNA levels, and increased p53 protein levels. Gene expression changes induced in HKc/DR by anti-SIX1 shRNA were indicative of mesenchymal-epithelial transition (EMT) and changes in TGF-beta signaling. We conclude that HPV16-transformed cells depend on SIX1 for survival, continuous HPV16 E6/E7 gene expression and EMT.

2019-08-20 | GSE126926 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data