Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells pancreatic tumor cell line MiaPaca2 was treated with a supernatant of pancreatic stellate cells and harvested hourly at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays.
Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells pancreatic tumor cell line MiaPaca2 was treated with a supernatant of pancreatic stelalte cells, primed with cumulative TC-supernatant (of 8 tumor cell lines, TC) and harvested hourly at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays.
Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells Primary pancreatic Stellate cells (PSC) were treated with a cumulative supernatant of pancreatic tumor cell lines (n=8) and harvested at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays. The 8 tumor cell lines are pancreatic ductal adenocarcinoma lines: AsPC1, BxPC3, Capan1, Colo357, MiaPaca2, Panc1, Su8686, and T3M4
Project description:Capan1 (well differentiated pancreatic cancer cell line) was co-cultured with pancreatic stellate cell line (PS1) embedded in a 3D organotypic model and gene expression was analysed in comparison to cancer cells cultured alone without stellate cells.
Project description:Capan1 (well differentiated pancreatic cancer cell line) was co-cultured with pancreatic stellate cell line (PS1) embedded in a 3D organotypic model and gene expression was analysed in comparison to cancer cells cultured alone without stellate cells. Pancreatic stellate cells were embedded within a gel matrix composing collagen type I and Matrigel, and cancer cells were seeded on top. The gel was lifted on to metal grid after 24 hour and fed from below. Gels were harvested on day 10 and frozen sections obtained. The cancer cell layer on top of the gel was captured by laser microdissection for RNA extraction.
Project description:We and others have shown that AGR2 is frequently upregulated during the development of pancreatic cancer. We used microarray to look at the target genes regulated by AGR2 in pancreatic cancer cell lines FA6 and MiaPaCa2. Keywords: gene knock-down, overexpression We transiently down-regulated AGR2 expression in FA6 pancreatic cancer cells using INTERFERin transfection reagent and either AGR2 siRNA or non-targeting control siRNA for 48 hours. RNA was extracted and hybridized on Affymetrix microarrays. We looked for new target genes regulated by AGR2. We generated stable cell lines by introducing control vector pCEP4 or AGR2 overexpressing vector pCEP4-AGR2 into the pancreatic cancer cell line MiaPaCa2, single cell clones were then isolated. RNA was extracted and hybridized on Affymetrix microarrays.We looked for new target genes regulated by AGR2.
Project description:Pancreatic stellate cells are a kind of fibroblasts present in the pancreas and are the cells of origin of cancer-associated fibroblasts. In our previous study, we demonstrated the presence of Cxcl13-positive pancreatic stellate cells as a subpopulation of pancreatic stellate cells. In their genetic profiling, they were predicted to have anti-tumor effects, but their behavior in pancreatic cancer tissue in vivo is unknown. Whole transcriptome analysis was performed to identify genes altered in tumors in which Cxcl13-positive pancreatic stellate cells were allogeneically subcutaneously transplanted with a pancreatic cancer cell line. In addition to the Cxcl13-positive pancreatic stellate cells, tumors transplanted with myofibroblastic pancreatic stellate cells were also subjected to whole transcriptome analysis.
Project description:Our study has shown that ARHGEF10 is a putative tumor suppressor in pancreatic ductal adenocarcinoma. To determine its functional mechanism, we perfomed microarray gene expression analysis of two pancreatic cancer cell line models of ARHGEF10 expression : MiaPACA2 cells in which ARHGEF10 was stably overexpressed, and Hs766T cells in which ARHGEF10 expression had been stably knocked down by short hairpin RNAs.
