Expression data from pancreatic cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE21163 | GEO | 2010/04/02
SECONDARY ACCESSION(S): PRJNA126617
REPOSITORIES: GEO
Similar Datasets
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 We compared the gene expression profiles of 6 pancreatic cancer cell lines (panc215, A32-1, A38-5, panc2.5, panc2.8, and panc3.014), to the non-neoplastic pancreas cell line, HPDE. We also compared the baseline gene expression of the pancreatic cancer cell lines to expression patterns after treatment with 5-aza-dC alone, TSA alone, and to a combination of 5-aza-dC/TSA.
2010-04-14 | E-GEOD-21163 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to facilitate identification of novel tumor suppressor genes using an integrative genomics approach Genome wide DNA methylation profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to identify novel tumor suppressor genes
2012-11-01 | GSE40097 | GEO
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:Genome wide expression profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to facilitate identification of novel tumor suppressor genes using an integrative genomics approach Genome wide expression profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to facilitate identification of novel tumor suppressor genes using an integrative genomics approach
2012-11-01 | GSE40098 | GEO
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:Genome wide DNA methylation profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to facilitate identification of novel tumor suppressor genes using an integrative genomics approach Genome wide DNA methylation profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to identify novel tumor suppressor genes Bisulphite converted DNA from the 21 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip
2012-11-01 | E-GEOD-40097 | biostudies-arrayexpress
Project description:Genome wide expression profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to facilitate identification of novel tumor suppressor genes using an integrative genomics approach Genome wide expression profiling of 20 PDAC cell lines and an immortalized non-malignant pancreatic duct cell line (HPDE) to facilitate identification of novel tumor suppressor genes using an integrative genomics approach RNA from the 21 samples was converted to Cy3 labeled cRNA and hybridized to the array; arrays were processed with GenePix software and median array normalization was performed
2012-11-01 | E-GEOD-40098 | 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-2’-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 “methyl-CpG targeted transcriptional activation (MeTA)” 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-2’-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 “MeTA” 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 “MeTA” 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.
2012-12-11 | GSE26215 | GEO
Project description:We have run a shotgun proteomic analysis of cell lysates from pancreatic cancer cell lines (PANC-1, PaCa-44, MIA PaCa-2 and BxPC-3) vs. normal epithelial ductal pancreatic cells (HPDE) in LC-MS/MS. No labelling was performed and digestion was done with Trypsin/Lys-C mix endoproteinase.
2020-02-07 | MSV000084935 | MassIVE
Project description:We have run shotgun and PRM proteomic analysis of cellular proteome and secretome from pancreatic cancer cell lines (PANC-1, PaCa-44, MIA PaCa-2 and BxPC-3) vs. normal epithelial ductal pancreatic cells (HPDE) in LC-MS/MS. Stable isotopic labelling was performed and digestion was done with Trypsin/Lys-C mix endoproteinase.
2021-10-21 | MSV000088250 | MassIVE