Differentially expressed cellular genes in non-tumorigenic and tumorigenic HPV18 positive HeLa x fibroblast hybrid cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE14052 | GEO | 2013/11/27
SECONDARY ACCESSION(S): PRJNA112415
REPOSITORIES: GEO
Similar Datasets
Project description:Identification of genes differentially expressed in tumorigenic compared to non-tumorigenic, HPV18 positive cells Keywords: ordered We used microarrays to identify genes differentially expressed in tumorigenic HeLa x fibroblast hybrid cells (CGL3) and parental HeLa cells compared to non-tumorigenic HeLa x fibroblast hybrid cells (444). Gene expression profiles of proliferating cells under cell culture conditions were compared to identify differential gene expression patterns of upregulated and downregulated mRNA expression patterns of tumorigenic CGL3 and HeLa cells versus non-tumorigenic 444 cells..
2013-11-27 | E-GEOD-14052 | biostudies-arrayexpress
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
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 HPV18 E7 or the HPV18 E7 R84S variant.
2020-06-09 | GSE150201 | GEO
Project description:Most of the cervical cancers are caused by human papillomavirus (HPV) infection. It has been known that, in HeLa cells, HPV18 viral genome is integrated at chromosome 8q24.21 and activates transcription of proto-oncogene c-Myc. However, the mechanism of how the integrated HPV fragment exhibits transcription activation function has not been fully elucidated. In this study, we found that HPV18 transcripts themselves have an enhancer RNA-like function to activate their proximal genes including CCAT1-5L and c-Myc. We showed that the human genome-integrated HPV18 genes are activated by transcription coregulators BRD4, Mediator. The transcribed HPV18 RNAs form a liquid-like condensate at chromosome 8q24.21 locus, which in turn accumulates RNA polymerase II. Moreover, we identified uncharacterized transcript from Upstream Region of CCAT1-5L, named URC. The URC RNA is transcribed as a chimera RNA with HPV18 and is composed of 3'-untranslated region of HPV18 transcript. We found that the URC contributes to stabilization of HPV18 RNAs by supplying a poly-adenylation site for HPV18 transcript. Our findings suggest that HPV18 integration at 8q24.21 locus causes HPV18-URC chimera RNA and promotes tumorigenesis through RNA-based liquid droplet formation.
2024-12-31 | GSE249929 | GEO
Project description:In order to study the molecular mechanism of HPV18 carcinogenesis, we used conditional reprogramming technique to culture normal cervical epithelial cells, cervical intraepithelial Neoplasia HPV18 cells and patient-derived cervical cancer cell lines for 24 h and stimulated with estradiol for 24 h,and collected total RNA samples for mRNA sequencing (RNA-SEQ). Then, Gene expression profiling was performed using RNA-seq data from six groups of cells.
2025-01-01 | GSE234041 | GEO
Project description:Apoptosis is a form of regulated cell death that plays a critical role in survival and developmental homeostasis. There are numerous reports on regulation of apoptosis by protein-coding genes as well as small non-coding RNAs, such as microRNAs. However, there is no comprehensive investigation of circular RNAs (circRNA) that are differentially expressed under apoptotic conditions. We have performed a transcriptomics study in which we first triggered apoptosis in HeLa cells through treatment with four different agents, namely cisplatin, doxorubicin, TNF-α and anti-Fas mAb. Total RNAs isolated from control as well as treated cells were treated with RNAse R to eliminate the linear RNAs. The remaining RNAs were then subjected to deep-sequencing to identify differentially expressed circRNAs. Interestingly, some of the dys-regulated circRNAs were found to originate from protein-coding genes well-documented to regulate apoptosis. A number of candidate circRNAs were validated with qPCR with or without RNAse R treatment as well. We then took advantage of bioinformatics tools to investigate the coding potential of differentially expressed RNAs. Additionally, we examined the candidate circRNAs for the putative miRNA-binding sites and their putative target mRNAs. Our analyses point to a potential for circRNA-mediated sponging of miRNAs known to regulate apoptosis. In conclusion, this is the first transcriptomics study that provides a complete circRNA profile of apoptotic cells that might shed light onto the potential role of circRNAs in apoptosis.
| S-EPMC6424894 | biostudies-literature
Project description:Yersinia enterocolitica is a facultative intracellular pathogen and a causative agent of yersiniosis, which can be contracted by ingestion of contaminated food. Yersinia secretes virulence factors to subvert critical pathways in the host cell. In this study we utilized shotgun label-free proteomics to study differential protein expression in epithelial cells infected with Y.enterocolitica. We identified a total of 551 proteins, amongst which 42 were downregulated (including Prostaglandin E Synthase 3, POH-1 and Karyopherin alpha) and 22 were upregulated (including Rab1 and RhoA) in infected cells. We validated some of these results by western blot analysis of proteins extracted from Caco-2 and HeLa cells. The proteomic dataset was used to identify host canonical pathways and molecular functions modulated by this infection in the host cells. This study constitutes a proteome of Yersinia-infected cells and can support new discoveries in the area of host-pathogen interactions.Statement of significance of the studyWe describe a proteome of Yersinia enterocolitica-infected HeLa cells, including a description of specific proteins differentially expressed upon infection, molecular functions as well as pathways altered during infection. This proteomic study can lead to a better understanding of Y. enterocolitica pathogenesis in human epithelial cells.
| S-EPMC5505629 | biostudies-literature
Project description:We perfomed RNA-seq analysis using HPV18-postive HeLa cells for HPV integration and expression analyses
2021-03-25 | GSE165475 | GEO
Project description:Background: Skin Cutaneous Melanoma (SKCM) is known as an aggressive malignant cancer, which could be directly derived from melanocytic nevi. However, the molecular mechanisms underlying the malignant transformation of melanocytes and melanoma tumor progression still remain unclear. Increasing research showed significant roles of epigenetic modifications, especially DNA methylation, in melanoma. This study focused on the identification and analysis of methylation-regulated differentially expressed genes (MeDEGs) between melanocytic nevus and malignant melanoma in genome-wide profiles. Methods: The gene expression profiling datasets (GSE3189 and GSE114445) and gene methylation profiling datasets (GSE86355 and GSE120878) were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and differentially methylated genes (DMGs) were identified via GEO2R. MeDEGs were obtained by integrating the DEGs and DMGs. Then, a functional enrichment analysis of MeDEGs was performed. STRING and Cytoscape were used to describe the protein-protein interaction (PPI) network. Furthermore, survival analysis was implemented to select the prognostic hub genes. Next, we conducted gene set enrichment analysis (GSEA) of hub genes. To validate, SKCM cell culture and lentivirus infection was performed to reveal the expression and behavior pattern of KIF2C. Patients and specimens were collected and then immunohistochemistry (IHC) staining was conducted. Results: We identified 237 hypomethylated, upregulated genes and 182 hypermethylated, downregulated genes. Hypomethylation-upregulated genes were enriched in biological processes of the oxidation-reduction process, cell proliferation, cell division, phosphorylation, extracellular matrix disassembly and protein sumoylation. Pathway enrichment showed selenocompound metabolism, small cell lung cancer and lysosome. Hypermethylation-downregulated genes were enriched in biological processes of positive regulation of transcription from RNA polymerase II promoter, cell adhesion, cell proliferation, positive regulation of transcription, DNA-templated and angiogenesis. The most significantly enriched pathways involved the transcriptional misregulation in cancer, circadian rhythm, tight junction, protein digestion and absorption and Hippo signaling pathway. After PPI establishment and survival analysis, seven prognostic hub genes were CKS2, DTL, KIF2C, KPNA2, MYBL2, TPX2, and FBL. Moreover, the most involved hallmarks obtained by GSEA were E2F targets, G2M checkpoint and mitotic spindle. Importantly, among the 7 hub genes, we found that down-regulated level of KIF2C expression significantly inhibited the proliferative ability of SKCM cells and suppressed the metastasis capacity of SKCM cells. Conclusions: Our study identified potential aberrantly methylated-differentially expressed genes participating in the process of malignant transformation from nevus to melanoma tissues based on comprehensive genomic profiles. Transcription profiles of CKS2, DTL, KIF2C, KPNA2, MYBL2, TPX2, and FBL provided clues of aberrantly methylation-based biomarkers, which might improve the development of precision medicine. KIF2C plays a pro-tumorigenic role and potentially inhibited the proliferative ability in SKCM.
| S-EPMC9387026 | biostudies-literature
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