Expression data from pancreatic cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Audrey Vincent
PROVIDER: E-GEOD-21163 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Expression data from pancreatic cancer cell lines and non-neoplastic pancreatic cell line HPDE To identify genes epigenetically silenced and regulated in pancreatic cancer
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Project description:Gene expression analysis of 5-aza-dC treated pancreatic cancer associated fibroblasts To identify genes silenced by methylation in pancreatic CAFs, we performed gene expression profiling on 5-aza-dC treated pancreatic cancer associated fibroblast cultures using Affymetrix Exon arrays. We analyzed 5 untreated and 5-aza-dC-treated pancreatic cancer associated fibroblast cultures using the Affymetrix Human Exon 1.0 ST platform. Gene expression levels were compared using Partek (version 6.3beta).
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Project description:Gene expression analysis of 5-aza-dC treated pancreatic cancer associated fibroblasts To identify genes silenced by methylation in pancreatic CAFs, we performed gene expression profiling on 5-aza-dC treated pancreatic cancer associated fibroblast cultures using Affymetrix Exon arrays.
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Project description:Transcriptome analysis in head and neck cancer cell lines, FaDu and UMSCC47 with and without 5-aza'2-deoxycytidine(Aza)/trichostatin A(TSA) treatment.
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Project description:DNA methylation analysis in oropharyngeal squamous carcinoma(OPSCC) samples, oropharyngeal non-cancerous mucosa samples and head and neck cancer cell lines, FaDu and UMSCC47 before and after 5-aza'2-deoxycytidine(Aza)/trichostatin A(TSA) treatment. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites. Samples included 13 OPSCC samples, 4 non-cancerous mucosa samples and 2 FaDu with and without Aza/TSA treatment and 2 UMSCC47 with and without Aza/TSA treatment.
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Project description:Global gene expression profiling on replicates of 9 pancreatic cancer cell lines (L3.6pl, BxPC3, CFPAC, SU8686, Panc-1, Hs766T, AsPC1, MIAPaca-2, MPanc 96) and normal HPDE cells was performed to elucidate multi-drug sensitivity/ resistance. Keywords: D microarray (Illumina human 2) Duplicates of 9 pancreatic cancer cell lines and 1 normal HPDE cell line were used. Microarray experiment and data analysis were done at Dept. of Urology, MDACC (Houston, USA).
2010-06-24 | E-GEOD-15550 | biostudies-arrayexpress
Project description:Transcriptional silencing associated with aberrant promoter hypermethylation is a common mechanism of inactivation of tumor suppressor genes in cancer cells. To profile the genes silenced by hypermethylation in prostate cancer, we screened an expression microarray for genes reactivated in the LNCaP, DU-145, PC-3 and MDA2b prostate tumor cell lines after treatment with the demethylating drug 5-aza-2 deoxycytidine (5Aza-dC) and histone deacetylation inhibiting drug trichostatin A (TSA).
2011-01-31 | E-GEOD-18573 | biostudies-arrayexpress
Project description:Identification and characterization of epigenetically silenced genes is very important for cancer research. Particularly, information of hypermethylated genes provides clues to understand roles of epigenetics in tumorigeneses, and genes frequently methylated in a tumor-specific manner can be used as tumor markers. DNA methylation inhibitors such as 5-aza-cytidine or 5-aza-2M-bM-^@M-^Y-deoxycytidine were widely used to search epigenetically silenced genes. However, these inhibitors frequently upregulate genes whose promoters remain unmethylated. We tried to improve the specificity and sensitivity in detecting such methylation-mediated silenced genes in cancer and successfully developed a new method termed M-bM-^@M-^\methyl-CpG targeted transcriptional activation (MeTA)M-bM-^@M-^] by using a transcriptional activating fragment with a methyl-CpG binding domain (MBD) that specifically recognizes and binds to methylated DNAs. Because MBD proteins in fact mediate transcriptional repression of tumor suppressor genes associated with promoter hypermethylation in cancer, MeTA is thought to be one of the ideal methods to search such genes. In the present study, we applied this method to three representative pancreatic cancer cell lines, AsPC-1, MIA PaCa-2, and PANC-1, with a normal pancreatic ductal epithelial cell line HPDE (as the control). All of these cell lines have already been analyzed their expression profiles by 5-aza-2M-bM-^@M-^Y-deoxycytidine. We first analyzed the expression of five genes by RT-PCR with Southern hybridization, NEFH, NPTX2, SFRP1, TIMP3, and UCHL1; these genes are known to be methylated in at least any one of these cancer cell lines. Upregulation by M-bM-^@M-^\MeTAM-bM-^@M-^] was confirmed in all of these genes. Then we searched for upregulated-genes, by two-folds or more, in all the three cancer cell lines after MeTA; nineteen such upregulated genes were identified. Among these, sixteen genes except NEFH, HOXA9, and CLDN5 have not been reported previously using the conventional DNA methylation inhibitors. Methylation status of two genes, SLC32A1 and CSMD2, were further analyzed by methylation-specific PCR and found that SLC32A1 and CSMD2 were methylated in 100% (21/21) and 83% (15/18) pancreatic cancer cell lines analyzed, respectively. Our results suggest that M-bM-^@M-^\MeTAM-bM-^@M-^] is a highly efficient method to isolate methylation-mediated transcriptionally silenced genes in human pancreatic cancer and that this method can be applied to other types of human cancer. Three representative pancreatic cancer cell lines, AsPC-1, MIA PaCa-2, and PANC-1, with a normal pancreatic ductal epithelial cell line HPDE (as the control) were transfected with pcDNA6/myc-His vector or pcDNA6-3xFLAG-NFkB (AD)-MBD and were harvested 48 h after transfection.
2012-12-11 | E-GEOD-26215 | biostudies-arrayexpress
Project description:Epigenetic changes largely contribute to the regulation of gene expression in cancer cells. DNA methylation is part of the epigenetic gene regulation complex which is relevant for the pathogenesis of cancer. We performed a genome-wide search for methylated CpG islands in tumors and corresponding non-malignant lung tissue samples of 101 stage I-III non-small cell lung cancer (NSCLC) patients by combining methylated DNA immunoprecipitation and microarray analysis using NimbleGenM-BM-4s 385K Human CpG Island plus Promoter arrays. By testing for differences in methylation between tumors and corresponding non-malignant lung tissues, we identified 298 tumor-specifically methylated genes. From many of these genes epigenetic regulation was unknown so far. Gene Ontology analysis revealed an over-representation of genes involved in regulation of gene expression and cell adhesion. Expression of 182 of 298 genes was found to be upregulated after 5-aza-2M-BM-4-deoxycytidine (Aza-dC) and/or trichostatin A (TSA) treatment of 3 NSCLC cell lines by Affymetrix microarray analysis. In addition, methylation of selected genes in primary NSCLCs and corresponding non-malignant lung tissue samples were analyzed by methylation-sensitive high resolution melting analysis (MS-HRM). Our results obtained by MS-HRM analysis confirmed our data obtained by MeDIP-chip analysis. Moreover, by comparing methylation results from MeDIP-chip analysis with clinico-pathological parameters of the patients we observed methylation of HOXA2 as potential parameter for shorter disease-free survival of NSCLC patients. In conclusion, using a genome-wide approach we identified a large number of tumor-specifically methylated genes in NSCLC patients. Our results stress the importance of DNA methylation for the pathogenesis of NSCLCs. Overall, samples of 3 untreated, with Aza-dC treated and with Aza-dC/TSA treated NSCLC cell lines were hybridized to Affymetrix HG-U133_plus_2.0 microarrays (18 in total).
2012-11-26 | E-GEOD-32496 | biostudies-arrayexpress
Project description:Blocking histone deacetylation with trichostatin A (TSA) or blocking cytosine methylation using 5-aza-2'-deoxycytosine (aza-dC) can derepress silenced genes in multicellular eukaryotes, including animals and plants. We questioned whether DNA methylation and histone deacetylation overlap in the regulation of endogenous plant genes by monitoring changes in expression of ~7800 Arabidopsis thaliana genes following treatment with azadC, TSA, or both chemicals together. RNA levels for ~4% of the genes were reproducibly changed 3-fold or more by at least one treatment. Distinct subsets of genes are up-regulated or down-regulated in response to aza-dC, TSA, or simultaneous treatment with both chemicals, with little overlap among subsets. Surprisingly, the microarray data indicate that TSA and aza-dC are often antagonistic rather than synergistic in their effects. Analysis of green fluorescent protein transgenic plants confirmed this finding, showing that TSA can block the up-regulation of silenced green fluorescent protein transgenes in response to aza-dC or a ddm1 (decrease in DNA methylation 1) mutation. Our results indicate that global inhibition of DNA methylation or histone deacetylation has complex, nonredundant effects for the majority of responsive genes and suggest that activation of some genes requires one or more TSA-sensitive deacetylation events in addition to cytosine demethylation.
2007-05-10 | E-SMDB-4105 | biostudies-arrayexpress