Yarrow and marigold extracts and their effect in pancreatic cancer cells [CAL]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE124042 | GEO | 2018/12/19
REPOSITORIES: GEO
Similar Datasets
Project description:determine the molecular effect of yarrow and marigold supercritical extracts in gene expression of pancreatic cancer cells (MIA PaCa-2)
2018-12-19 | GSE124043 | GEO
Project description:Yarrow and marigold extracts and their effect in pancreatic cancer cells [CAL]
| PRJNA510608 | ENA
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:No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. MicroRNAs (miR) are epigenetic gene regulators with tumorsuppressive or oncogenic roles in various carcinomas. This study assesses chemoresistant PDAC for its specific miR expression pattern. Gemcitabine-resistant variants of two mutant p53 human pancreatic adenocarcinoma cell lines were established. MicroRNA screening was investigated by microarray. Gemcitabine-resistant PANC-1 (PANC-1-GR) and MIA-PaCa-2 (MIA-PaCa-2-GR) cell clones were produced by exposing the parental cells to repeated pulsatile gemcitabine treatment over 3 days with constant sublethal concentrations followed by recovery-periods with agent-free medium until the cells recovered exponentially. Parental PANC-1 cells were treated with 0.4µM gemcitabine cycles for approximately 9 months. Parental MIA-PaCa-2 cells were exposed to 0.06µM gemcitabine cycles for approximately 12 months. Affymetrix GeneChip miRNA microarrays (Affymetrix UK Ltd., High Wycombe, UK) were performed in parental and chemoresistant PANC-1 and MIA-PaCa-2 cells after 29 chemotherapy cycles using the manufacturers´ protocols. The samples were prepared from 1µg of total-RNA in accordance with the Affymetrix FlashTag Biotin HSR RNA Labeling Kit. The targets were hybridized overnight to Affymetrix GeneChip miRNA arrays. Following hybridization, the arrays were washed and stained using the Affymetrix GeneChip Fluidics Station 450 and scanned using the Affymetrix GeneChip Scanner 3000 7G. Microarray data quality was checked as recommended by the manufacturer and by the quality metrics in the Partek Genomics Suite software (Partek Inc., St. Louis, MO).
2015-11-03 | E-GEOD-74565 | biostudies-arrayexpress
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
Project description:This microarray is an analysis of differentially expressed genes in three pancreatic ductal adenocarcinoma cell lines treated with LXR-agonist GW 3965. We first report that GW 3965 has antiproliferative effects in three PDAC cell lines. This microarray was designed to identify key mechanisms of the antiproliferative effect of LXR agonists within pancreatic cancer cell lines. Total RNA obtained from BxPC-3, MIA-PaCa-2, and PANC-1 pancreatic cancer cells grown in culture treated GW 3965 or ethanol (vehicle control) for 72 hours.
2014-04-15 | E-GEOD-51656 | biostudies-arrayexpress
Project description:MiRNAs differentially expressed in normal pancreatic cell line (Human Pancreatic Ductal Epithelial cell line) vs MIA PaCa-2 (Pancreatic cancer cell line) were first identified by profiling >1900 miRNAs using an array approach. Subsequently, miRNAs differentially expressed in DZNep treated cells (as compared to untreated) were also identified. We also checked for miRNA changes with gemcitabine treatment as well as combination treatment.
2016-09-03 | GSE86383 | GEO
Project description:We used time-dependent spheroidal cultures of pancreatic cancer cells to investigate how spatiotemporal regulation in spheroids induces epithelial-mesenchymal plasticity (EMP). We generated a round bottom spheroidal model using M-NM-23 integrin-negative pancreatic cancer cells in 2D conventional monolayer cultures, and compared the expression of integrin signaling-related genes that induce spheroidal geometry to determine if spheroidal geometry induces integrin switching. To identify the potential genes whose expression changed in response to culture conditions, we performed microarray analysis of gene expression in human MIA PaCa-2 cells grown under monolayer and spheroid culture conditions for 6 days and 13 days.
2014-08-06 | E-GEOD-60139 | biostudies-arrayexpress
Project description:The molecular mechanisms underlying exceptional radioresistance in pancreatic cancer remain elusive. In the present study, we established a stable radioresistant pancreatic cancer cell line MIA PaCa-2-R by exposing the parental MIA PaCa-2 cells to fractionated ionizing radiation (IR). Systematic proteomics and bioinformatics comparison of protein expression in MIA PaCa-2 and MIA PaCa-2-R cells revealed that several growth factor- and cytokine-mediated pathways, including the OSM/STAT3, PI3K/AKT and MAPK/ERK pathways, were activated in the radioresistant cells, leading to enhanced cell migration, invasion and epithelial-mesenchymal transition (EMT), and inhibition of apoptosis. We focused functional analysis on one of the most upregulated proteins in the radioresistant cells, CD73, which is a cell surface protein that is overexpressed in a variety types of cancer. Ectopic overexpression of CD73 in the parent cells resulted in radioresistance and conferred resistance to IR-induced apoptosis. Knockdown of CD73 resensitized the radioresistant cells to IR and IR-induced apoptosis. The effect of CD73 on radioresistance and apoptosis is independent of the enzymatic activity of CD73. Further studies suggest that CD73 confers acquired radioresistance in pancreatic cancer cells at least in part through inactivating proapoptotic protein BAD via phosphorylation of BAD at Ser-136. Furthermore, we found that knockdown of CD73 in the radioresistant cells alone reverted the gene expression and phenotype of the radioresistant cells from those of mesenchymal-like cells to the ones of epithelial cells, demonstrating that CD73 upregulation is required for maintaining EMT in the radioresistant cells. Our results support the notion that the enhanced growth factor/cytokine signaling that promotes epithelial-mesenchymal plasticity, and acquisition of cancer stem-like cell properties contributes to acquired radioresistance in the residual surviving cells after fractionated irradiation, and that CD73 is a novel downstream factor of those enhanced signaling and acts to confers acquired radioresistance and maintains EMT in the radioresistant pancreatic cancer cells.
2019-12-31 | PXD012922 | Pride
Project description:Background: Pachymic acid (PA) is a purified triterpene extracted from medicinal fungus Poria cocos. In this paper, we investigated the anticancer effects of PA on human chemotherapy resistant pancreatic cancer cells. Methods: Gemcitabine-resistant pancreatic cancer cells PANC-1 and MIA PaCa-2 were used, along with a xenograft model of MIA PaCa-2 cells implanted in mice. Apoptosis was assessed by quantitation of cytoplasmic histone-associated DNA fragments and expression of cleaved PARP. Differential expression of genes was identified using comparative DNA microarray analysis. Protein levels were determined by immunoblotting. Toxicology studies in vivo were assessed by detecting pathological changes in organs and liver enzyme profiles in plasma. Tumor tissues were analyzed by quantification of apoptotic bodies, qRT-PCR and immunoblotting. Principal Findings: PA induced endoplasmic reticulum (ER) stress in chemotherapy resistant pancreatic cancer cells through activation of heat shock response and unfolded protein response related genes, which further triggered apoptosis. The involvement of ER stress was confirmed by increasing expression of XBP-1s, ATF4, Hsp70, CHOP and phospho-eIF2M-NM-1. Moreover, 25 mg kgM-bM-^HM-^R1 of PA significantly suppressed MIA PaCa-2 tumor growth in vivo without toxicity, which correlated with induction of apoptosis, ER stress related genes and proteins expression. Conclusions: Growth inhibition and induction of apoptosis by PA in chemotherapy resistant pancreatic cancer cells were associated with ER stress activation both in vitro and in vivo. Pancreatic cancer cell line treated with pachymic acid vs. control (untreated)
2014-12-12 | E-GEOD-64111 | biostudies-arrayexpress