Homo sapiens immortalized MSCs: KP vs. 3A6
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: E-GEOD-23936 | BioStudies |
REPOSITORIES: biostudies
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Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs. Two-condition experiment, KP MSCs vs. 3A6 MSCs.
2011-08-24 | E-GEOD-23936 | ArrayExpress
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
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Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs. One-condition experment, gene expression of 3A6
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Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs. One-condition experment, gene expression of 3A6
2010-09-25 | E-GEOD-24338 | ArrayExpress
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2010-09-25 | GSE24338 | GEO
Project description:Cervical cancer is the most fourth common cancer in women worldwide. The E6 and E7 high-risk human papillomavirus (HPV) types are the main cause of this cancer. Several studies have revealed that promoter methylation of tumor suppressor genes is induced by HPV E7. Recently, it was found that HPV16-E7 and the DNA methyltransferase 1 complex could bind at the cyclin A1 (CCNA1) promoter, resulting in CCNA1 promoter methylation. Therefore, there is a need to study other tumor suppressor genes for which HPV may induce promoter methylation. The present study investigated whether HPV induced cell adhesion molecule 1 (CADM1) and death associated protein kinase 1 (DAPK1) promoter methylation. C33a (no HPV infection) and SiHa (HPV 16 infection) cell lines were used for methylation status and expression observation. It was found that CADM1 and DAPK1 promoter methylation, no expression of CADM1 and decreased expression of DAPK1, was presented in SiHa cells. While no promoter methylation of these two genes was observed in C33a cells, with positive expression of the genes. It was subsequently investigated whether E6 and/or E7 could induce promoter methylation and decrease the expression of these two genes. Methylation-specific primer PCR and quantitative PCR were performed to elucidate the promoter methylation status and expression of CADM1 and DAPK1 in C33a cells transfected with HPV16 E6-PCDNA3 or HPV16 E7-PCDNA3.1 myc-his, compared to empty vector-transfected cells. The results showed that HPV E7 could induce CADM1 promoter methylation and decrease the gene expression in HPV E7 transfected C33a cells, while HPV E6 could induce DAPK1 promoter methylation and decrease its expression in C33a cells transfected with HPV E6. Finally, the mechanism by which HPV E7 induced CADM1 promoter methylation was observed by performing chromatin immunoprecipitation; the data showed that E7 induced CADM1 methylation by the same mechanism as that for CCNA1, by binding at the CADM1 promoter, resulting in the subsequent reduction of its expression in cervical cancer.
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Project description:BACKGROUND: Recently, transcriptional gene silencing induced by small interfering RNA (siRNA) was found in mammalian and human cells. However, previous studies focused on endogenous genes. METHODS: In this study, we designed siRNA targeting the promoter of human papillomavirus 16 E6/E7 and transfected it into the cervical cancer cell line, SiHa. E6 and E7 mRNA and protein expression were detected in cells treated by promoter-targeting siRNA. Futhermore, cellular growth, proliferation, apoptosis and senescence were detected. Thereafter, we investigated promoter DNA methylation and histone methylation status in cells treated with promoter-targeting siRNA. RESULTS: We found that E6/E7 mRNA and protein were simultaneously reduced, cell growth and proliferation were inhibited and cell death, especially senescence, was remarkably increased. Meanwhile, we also found a significantly increasing histone H3-Lys9 methylation on the promoter when E6/E7 gene expression was inhibited. INTERPRETATION: Our findings suggest that promoter-targeting siRNA effectively and simultaneously knocks down both extraneous HPV 16 E6 and E7 at the transcriptional level, and consequently inhibits proliferation and induces death in HPV 16-infected cells. This transcriptional repression is probably induced by histone modification rather than by alteration of DNA methylation.
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Project description:Assess gene expression patterns upon HOXA9 ectopic expression in U87MG GBM cell line and hTERT/E6/E7 immortalized human astrocytes, and HOXA9 silencing in U251 and GBML18 GBM cell lines. U87MG and hTERT/E6/E7 were retrovirally-infected with an MSCV control vector (MSCV-Control) or with a construct containing the coding region of HOXA9 (MSCV-HOXA9), resulting in U87MG-Control, U87MG-HOXA9, hTERT/E6/E7-Control and hTERT/E6/E7-HOXA9 cell lines. GBML18 and U251 cells were transfected with HOXA9 gene-specific shRNA sequences (shHOXA9) or a non-efective shRNA (shControl) in pGFP-V-RS plasmid, resulting in U251-shControl, U251-shHOXA9, GBML18-shControl and GBML18-shHOXA9 cell lines. Four experimental replicates for HOXA9 overexpression cell lines, and three for HOXA9 silencing cell lines were performed.
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Project description:Telomerase activation is critical for the immortalization of primary human keratinocytes by the high-risk HPV E6 and E7 oncoproteins, and this activation is mediated in part by E6-induction of the hTERT promoter. E6 induces the hTERT promoter via interactions with the cellular ubiquitin ligase, E6AP, and with the c-Myc and NFX-1 proteins, which are resident on the promoter. In the current study we demonstrate that E6 protein interacts directly with the hTERT protein. Correlating with its ability to bind hTERT, E6 also associates with telomeric DNA and with endogenous active telomerase complexes. Most importantly, E6 increases the telomerase activity of human foreskin fibroblasts transduced with the hTERT gene, and this activity is independent of hTERT mRNA expression. Unlike its ability to degrade p53, E6 does not degrade hTERT protein in vitro or in vivo. Our studies of E6/hTERT interactions also reveal that the C-terminal tagged hTERT protein, although incapable of immortalizing fibroblasts, does immortalize keratinocytes in collaboration with the viral E7 protein. Thus, E6 protein mediates telomerase activation by a posttranscriptional mechanism and these findings provide a model for exploring the direct modulation of cell telomerase/telomere function by an oncogenic virus and suggest its potential role in both neoplasia and virus replication.
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