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KRAS-induced transcription analysis in immortalized pancreatic cells

ABSTRACT: We utilized non-transformed, human pancreatic ductal epithelial (HPDE) cells, previously engineered with the E6 and E7 proteins of the HPV16 virus to emulate loss of p53 and inactivation of the Rb pathway, respectively. Given the frequent activation of KRAS (>90% PDAC tumors) and its early role in pancreatic neoplasia, we sought to engineer HPDE cells containing KRASG12D to provide the appropriate context in which to screen for novel drivers that might represent KRAS effectors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58055 | GEO | 2016/01/19

SECONDARY ACCESSION(S): PRJNA248764

REPOSITORIES: GEO

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KRAS-induced transcription analysis in immortalized pancreatic cells

Project description:We utilized non-transformed, human pancreatic ductal epithelial (HPDE) cells, previously engineered with the E6 and E7 proteins of the HPV16 virus to emulate loss of p53 and inactivation of the Rb pathway, respectively. Given the frequent activation of KRAS (>90% PDAC tumors) and its early role in pancreatic neoplasia, we sought to engineer HPDE cells containing KRASG12D to provide the appropriate context in which to screen for novel drivers that might represent KRAS effectors. The KRAS-induced transcription analysis was conducted using RNAs extracted from HPDE cells transduced with either control, wild-type KRAS or KRASG12D(pInducer) with or without DOX (100ng/ml) for 72 h, followed by hybridization of labeled cDNA onto Agilent arrays (Agilent G3 Human GE 8x60K) by the Baylor College of Medicine Genome Profiling Core Facility. multi-group comparison

2016-01-19 | E-GEOD-58055 | biostudies-arrayexpress

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

2013-11-27 | GSE14051 | 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

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

Modulation of microRNA-mRNA Target Pairs by Human Papillomavirus 16 Oncoproteins

Project description:The E6 and E7 proteins are the major oncogenic drivers encoded by high-risk human papillomaviruses (HPVs). While many aspects of the transforming activities of these proteins have been extensively studied, there are fewer studies that have investigated how HPV E6/E7 expression affects expression of cellular noncoding RNAs. The goal of our study was to investigate HPV16 E6/E7 modulation of cellular microRNA (miR) levels and to determine the potential consequences on cellular gene expression. We performed deep sequencing of small and large cellular RNAs in primary, undifferentiated cultures of human foreskin keratinocytes (HFKs) with stable expression of HPV16 E6/E7 or a control vector. After integration of the two data sets we identified 51 differentially expressed cellular miRs associated with modulation of 1,456 potential target mRNAs in HPV16 E6/E7 expressing HFKs. We discovered that the degree of differential miR expression in HFKs expressing HPV16 E6/E7 was not necessarily predictive of the number of corresponding mRNA targets or the potential impact on gene expression. Additional analyses of the identified miR-mRNA pairs suggest modulation of specific biological activities and biochemical pathways. Overall, our study supports the model that perturbation of cellular miR expression by HPV16 E6/E7 importantly contributes to the rewiring of cellular regulatory circuits by the high-risk HPV E6 and E7 proteins that contribute to oncogenic transformation.

2017-01-17 | GSE92496 | GEO

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

Gene expression of cervical cells and immortalized keratinocytes transfected with whole genomes of HPV16 and HPV18

Project description:Human ectocervical and endocervical cells immortalized by HPV16 E6/E7 (designated as Ect and End, respectively) and normal human immortalized keratinocytes (NIKS), were transfected with whole genomes of HPV16 or HPV18, and were subsequently grown in standard monolayer culture until passage 2. Total RNAs were extracted and subjected to TORAY 3D-gene analysis service using the 3D-Gene Human Oligo chip 25K (TORAY, Tokyo, Japan).

2019-08-01 | GSE131076 | GEO

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

Systematic analysis of IL-1 cytokine signaling by high-risk HPV oncoproteins

Project description:Human papillomavirus (HPV) E6 and E7 oncoproteins are expressed at all stages of HPV-mediated carcinogenesis and are essential drivers of cancers caused by high-risk HPV. Some of the activities of HPV E6 and E7, such as their interactions with host cellular tumor suppressors, have been characterized extensively. There is less information about how high-risk HPV E6 and E7 alter cellular responses to cytokines that are present in HPV-infected tissues and are an important component of the tumor microenvironment. We used several models of HPV oncoprotein activity to assess how E6 and E7 alter the cellular response to the pro-inflammatory cytokine IL-1beta. Models of early-stage HPV infection (human keratinocytes expressing HPV16 E6 and E7) and models of established HPV-positive head and neck cancers (patient-derived xenografts, head and neck cancer cell lines) exhibited similar dysregulation of IL-1 pathway genes and suppressed responses to IL-1beta treatment. Such overlap in cell responses supports that changes induced by HPV E6 and E7 early in infection could persist and contribute to a dysregulated immune environment throughout carcinogenesis. HPV E6 and E7 also drove the upregulation of several suppressors of IL-1 cytokine signaling, including SIGIRR, both in primary keratinocytes and in cancer cells. SIGIRR knockout was insufficient to increase IL-1beta-dependent gene expression in the presence of HPV16 E6 and E7, suggesting that multiple suppressors of IL-1 signaling contribute to dampened IL-1 responses in HPV16-positive cells.

2022-10-31 | GSE211730 | GEO

The impact of HPV16 and HPV18 E6/E7 oncogenes on gene expression in non-tumorigenic keratinocytes (HaCaT cells)

Project description:This analysis aimed to identify differentially expressed genes in non-tumorigenic keratinocytes transduced with E6/E7 oncogenes of HPV16 or 18. The working cell models were named HaCaT E6/E7 HPV16, HaCaT E6/E7 HPV18, and HaCaT pLVX (empty lentiviral vector) as controls. mRNA sequencing was performed on the Illumina NovaSeq 6000 platform by Novogene Bioinformatics Technology Co., Ltd, Beijing, China, with two independent replicate sequences for each cell model. Methodology: The bioinformatics pipeline analysis was executed as described below: Rstudio (v2023.06.1+524) and Galaxy (https://www.usegalaxy.orgaccessed on 15 August 2023) open-source platforms were used to analyze the Illumina raw data. The Quality Check was performed through the FastQC tool (v0.12.1); afterward, all the reads were processed by the Rsubread package (v2.14.2); at that point, the reads were trimmed and aligned to the Human Genome Reference (GRCh38.p14 v43). The resulting output was the BAM files, of which the number of reads was counted by the featureCounts tool (v2.0.3); at the final step, the Differential Expression Analysis was settled by DESeq2 tool (v2.11.40.8). The differential gene expression measurements were normalized by DESeq2´s median of ratios (median of ratio of gene counts relative to geometric mean per gene) method. All chemokine genes with an adjusted p-value (adj p) ≤ 0.05 and fold change (Log2FC) > 1 .5 or < -1.5 were selected as differentially expressed genes (DEGs). Some genes from the resulting outputs were validated through qPCR. Conclusions: Our study found 3296 differentially expressed genes in HaCaT E6/E7 HPV16 and 1943 in HaCaT E6/E7 HPV18. These results suggest that E6/E7 oncogenes from HPV16 and 18 can broadly modify transcriptomic expression.

2023-11-02 | GSE241704 | GEO

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