Expression data from pancreatic stellate cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE49583 | GEO | 2013/08/09
SECONDARY ACCESSION(S): PRJNA214664
REPOSITORIES: GEO
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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
2013-08-09 | E-GEOD-49583 | biostudies-arrayexpress
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
2013-08-09 | GSE49586 | GEO
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
2013-08-09 | GSE49584 | GEO
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.
2013-08-09 | E-GEOD-49584 | biostudies-arrayexpress
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.
2013-08-09 | E-GEOD-49586 | biostudies-arrayexpress
Project description:Human pancreatic stellate cells (HPSCs) are an essential stromal component and are the mediators of pancreatic ductal adenocarcinoma (PDAC) progression. Small extracellular vesicles (sEVs) are membrane-enclosed nanoparticles released from stellate cells adjacent to the PDAC. sEVs are believed to play a key role in cell-cell communications and may play a critical role in disease progression. The role of membrane proteins of HPSC sEVs in the PDAC tumor microenvironment is unclear and to date, there has not been a quantitative proteomic comparison of sEVs from normal pancreatic stellate cells (HPaStec) and from PDAC-associated stellate cells (HPSCs). We hypothesized there would be differences in sEVs secretion and membrane protein expression between the 2 conditions that might contribute to PDAC biology. To test these hypotheses, we isolated sEVs using ultracentrifugation followed by characterization by electron microscopy and Nanoparticle Tracking Analysis. HPSCs secreted more sEVs compared to HPaStec, and these sEVs were enriched with exosomal markers, which was confirmed by Western blotting and flow cytometry. HPSC-sEVs also restore the activation of normal stellate cells. Next, we showed that intact membrane-associated proteins may be essential for sufficient uptake of stellate cell sEVs by both normal epithelial and cancer cells. Importantly, we demonstrated that stellate cells in general modulate the cellular proliferations of pancreatic cancer cells although stellate cell sEVs did not change the proliferation of cancer cells. We then compared sEV proteins isolated from HPSCs and HPaStecs cells using liquid chromatography–tandem mass spectrometry. Most of the 1,481 protein groups identified were shared with the exosome database, ExoCarta (http://exocarta.org/; curated by the Mathivanan Lab). Eighty-seven protein groups were differentially expressed (selected by 2-fold difference and adjusted P value ≤ 0.05) between HPSC and HPaStec sEVs. HPSC sEVs contained dramatically more CSE1L, a poor prognostic marker for pancreatic cancer. In conclusion, our findings using mass spectrometry–based proteomics may direct further studies to understand the biology and role of protein composition of HPSC sEVs in PDAC progression or to develop novel strategies based on delivery of exosome cargo to PDAC tumor cells.
2023-03-11 | PXD030077 | Pride
Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the crosstalk between tumor hepatocytes and activated hepatic stellate cells (HSC) in liver cancer. This was adressed by using a coculture model system of HepaRG cell line (tumor hepatocytes, human), and LX2 cell line (HSC, human). By using genome-wide expression profiling, we demonstrated that hepatocyte-HSC crosstalk is bidirectional and results in the deregulation of functionally relevant gene networks. HepaRG and LX2 cells were cultured alone in serum- and DMSO-free William's E medium or together using 1 M-BM-5m pore size transwell inserts which allow diffusion of media components but prevent cell migration (BD Biosciences, San Jose, CA). Triplicate experiments were performed: HepaRG (culture versus coculture), LX2 (culture versus coculture).
2012-05-31 | E-GEOD-32565 | biostudies-arrayexpress
Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the crosstalk between tumor hepatocytes and activated hepatic stellate cells (HSC) in liver cancer. This was adressed by using a coculture model system of HepaRG cell line (tumor hepatocytes, human), and LX2 cell line (HSC, human). By using genome-wide expression profiling, we demonstrated that hepatocyte-HSC crosstalk is bidirectional and results in the deregulation of functionally relevant gene networks.
2012-06-01 | GSE32565 | GEO
Project description:This study used Illumina single-end RNA-sequencing to examine gene expression differences between 2 mouse-derived pancreatic stellate cell lines (PSC4, PSC5) grown either in 2D monolayers, as 3D quiescent cultures, or as 3D activated transwell cocultures with 2 mouse tumor-derived pancreatic ductal organoid lines (T4, T5). Mouse pancreatic stellate cell (PSC) lines were derived from the pancreata of wild-type C57Bl/6J mice. Mouse tumor organoid lines were derived from mouse pancreata containing pancreatic ductal adenocarcinoma (PDAC) from the KrasLSL-G12D; Trp53LSL-R162H; Pdx1-Cre mouse model. We measured genes differentially expressed among 2D, quiescent, and 3D activated PSCs that may reflect the expression changes of heterogeneous CAF population in pancreatic tumors.
2017-02-03 | GSE93313 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) progresses in an organ with a unique pH landscape, where the stroma acidifies after each meal. We hypothesized that disrupting this pH landscape during PDAC progression triggers pancreatic stellate cells (PSCs) and cancer-associated fibroblasts (CAFs) to induce PDAC fibrosis. We revealed that alkaline environmental pH is sufficient to induce PSC differentiation to a myofibroblastic phenotype. We then mechanistically dissected this finding focusing on the involvement of the Na+/H+ exchanger NHE1. Perturbing cellular pH homeostasis by inhibiting NHE1 with cariporide partially alters the myofibroblastic PSC phenotype. To show the relevance of this finding in vivo, we targeted NHE1 in murine PDAC (KPfC). Indeed, tumor fibrosis decreases when mice receive the NHE1-inhibitor cariporide in addition to gemcitabine treatment. Moreover, the tumor immune infiltrate shifts from granulocyte-rich to more lymphocytic. Taken together, our study provides mechanistic evidence on how the pancreatic pH landscape shapes pancreatic cancer through tuning PSC differentiation.
2023-09-18 | GSE223205 | GEO