Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Cela on pancreatic cancer cells

ABSTRACT: Effect of Some natural products on pancreatic cancer cells

ORGANISM(S): Homo sapiens

SUBMITTER: Mahmoud Youns

PROVIDER: E-MTAB-10185 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling by array to investigate effect of natural compounds on Panc1 cells compared to untreated controls

Project description:Here, we study the effect of some natural compounds on gene expression of pancreatic cancer cells (Panc-1) compared to untreated control.

2023-12-29 | E-MTAB-6586 | biostudies-arrayexpress

Genes activated by 5-aza-dC (DAC) in pancreatic cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-01 | E-GEOD-42366 | biostudies-arrayexpress

Genes activated by 5-aza-dC (DAC) in pancreatic cancer (KPC-Brca1) epithelial cells

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of malignant epithelial cells from a KPC-Brca1 mouse pancreatic carcinoma, with 0.5 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.

2013-01-01 | E-GEOD-42365 | biostudies-arrayexpress

Genes activated by 5-aza-dC (DAC) in pancreatic (KPC-Brca1) cancer-associated fibroblasts (CAFs)

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of cancer-associated fibroblasts (CAFs) from a KPC-Brca1 mouse pancreatic carcinoma, with 2 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.

2013-01-01 | E-GEOD-42364 | biostudies-arrayexpress

Multi-omics Study Reveals the Synergistic Anti-tumor Effects of Aspirin and Gemcitabine-based Chemotherapy on Pancreatic Cancer and the Underlying Mechanism

Project description:Pancreatic cancer is a highly malignant tumor that is well known for its poor prognosis. It has been reported that aspirin can reduce the risk of various cancers, but the potential role of aspirin and gemcitabine in pancreatic cancer pathogenesis and chemotherapy has not been studied. Therefore, we investigated their synergistic anti-tumor effects and explored the potential molecular mechanisms and biological functions underlying their inhibitory effects on the development of pancreatic cancer in the hope of identifying treatment-related or prognostic biomarkers for the effective treatment of pancreatic cancer.

2022-05-31 | PXD031910 | Pride

A pancreatic cancer cells spectral library and the phenotype analysis of gemcitabine-sensitive and -resistant pancreatic cell lines by the data-independent acquisition proteome strategy

Project description:Based on data-independent acquisition (DIA)-mass spectrometry (MS) strategies for in-depth proteome analysis, we established a high-coverage spectrum library from seven human pancreatic cell lines and evaluated performance of the library by exploring the molecular change between gemcitabine (GEM) sensitivity and resistance phenotypes .

2022-05-31 | PXD030948 | Pride

Establishment of pancreatic cancer cells spectral library based on data-independent acquisition strategy and the phenotype analysis of pancreatic cell lines of the sensitivity and resistance of gemcitabine

Project description:Based on data-independent acquisition (DIA)-mass spectrometry (MS) proteomics, we first established a high-coverage human pancreatic cells spectrum library. Furthermore, analyzed the sensitivity and drug resistance phenotypes to gemcitabine (GEM).

2022-05-31 | PXD031028 | Pride

Gene expression profiling of pancreatic cancer cell line BxPC-3 induced by PAR-2 AP

Project description:Protease-activated receptor-2 (PAR-2), a G protein-coupled receptor activated by trypsin and coagulant factors, plays broad spectrum of physiological and pathological roles especially in cancer development. In this study, we used PAR-2 activating peptide to mimic the action of trypsin to trigger PAR-2 signaling pathway and effects of PAR-2 activation on gene expression in human pancreatic cancer cell line BxPC-3 investigated by microarray analysis. Through DAVID bioinformatic resources, we observed that activated PAR-2-mediated genes are summarized to two different pathways, renal cell carcinoma and NFkB pathway. In renal cell carcinoma pathway, activated PAR-2 dysregulated hypoxia-inducible factors and its target genes, including glucose transporter 1 (GLUT1), transforming growth factor-b (TGF-b) and vascular endothelial growth factor-A (VEGF-A). In addition, activated PAR-2 induced MAPK signaling and transcriptional factors, such as JUN, MAP2K1 and ETS1. The regulation of these genes by PAR-2 assumed that PAR-2 signaling was associated with cancer progression. On the other hand, activated PAR-2 upregulated interleukin-1b (IL-1b) and toll-like receptor 4 (TLR4) related with NFkB activation, which indicated that PAR-2 signaling may cause cancer-related inflammation. In conclusion, PAR-2 may be a factor to regulate cancer progression and inflammation. Two-condition experiment, control cells vs PAR-2 AP-treated cells.

2013-04-30 | E-GEOD-44827 | biostudies-arrayexpress

Sodium arsenate response of wild type and slt2 deficient cells

Project description:Wild type (BY4741) Saccharomyces cerevisiae strains and their isogenic slt2 deficient counterparts, were treated for 2 hours with sodium arsenate 100 micromolar. Control (untreated) cells were also collected. Total RNA was extracted and analyzed by microarray hybridization. The data obtained from these experiments allows to determine those genes that are regulated by Slt2 activity after arsenate treatment. The experiments was designed as follows: Four types of samples were used: untreated wild type cells, treated wild type cells, untreated slt2- cells and treated slt2- cells. 3 independent replicates were performed for each experiment.

2010-07-25 | E-GEOD-17364 | biostudies-arrayexpress

Transcriptomic responses of human hepatocellular carcinoma cells (HepG2/C3A) to dust, flame retardants and dimethylbenzanthracene

Project description:Human HepG2/C3A cells were exposed to indoor dust reference material SRM2585; DMBA (dimethylbenzanthracene); HBCD (hexabromocyclododecane); two different mixtures of flame retardants (all dissolved in 0.1% DMSO) or 0.1% DMSO alone for 72h. RNA was prepared and labeled with Cy3 then hybridized to Agilent SurePrint G3 Human GE v2 8x60k Microarrays, Agilent design ID 039494.

2015-10-01 | E-MTAB-3324 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data