Browse
Submit Data
Databases
API
Help

Dataset Information

4 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative analysis of NRF2-responsive gene expression in AcPC-1 pancreatic cancer cell line.

ABSTRACT: NRF2 is a nuclear transcription factor activated in response to oxidative stress and related with metabolizing of xenotoxic materials and ABC transporter mediated drug resistance. We studied the expression of mRNAs under the siRNA-mediated knockdown of NRF2 and tBHQ-treated condition in AsPC-1 metastatic pancreatic cancer cell line to understand the AsPC-1 specific role(s) of NRF2 and further to investigate the relationship between drug resistance and metastatic plasticity and mobility of AsPc1. Here we show that the genes of aldo-keto reductases, cytochrome P450 family, aldehyde dehydrogenase, thioredoxin reductase, ABC transporter and epoxide hydrolase responsible for drug metabolism or oxidative stress concisely responded to NRF2 stabilization and knockdown of NRF2. In addition the expression of PIR, a candidate of oncogene and KISS1, a suppressor of metastasis were affected by NRF2 stabilization and knockdown. Our result provide comprehensive understanding of NRF2 target genes of drug response, oxidative stress response and metastasis in AsPc-1 metastatic pancreatic cancer cell line.

SUBMITTER: Yi YW

PROVIDER: S-EPMC4269820 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Expression data from pancreatic cancer cell line MiaPaca2

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.

| S-ECPF-GEOD-49586 | biostudies-other

Expression data from pancreatic cancer cell line MiaPaca2 [control]

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.

| S-ECPF-GEOD-49584 | biostudies-other

Gene expression analysis & Comparative genomic hybridization from Lung cancer Cell lines

Project description:Gene expression and Comparative genomic hybridization (CGH) microarrays performed in a set of 8 Lung cancer Cell lines. The search for oncogenes is becoming increasingly important in cancer genetics because they constitute suitable targets for therapeutic intervention. To identify novel oncogenes, activated by gene amplification, we performed high-resolution CGH (Comparative Genome Hybridization) analysis on cDNA microarrays and compared DNA copy number and mRNA expression levels in lung cancer cell lines. We have performed both microarrays (expression and CGH) in a set of 8 human lung cancer cell lines: Calu3, H23, H441, A427, H522, A549, H1299, H2126.

| S-ECPF-GEOD-14079 | biostudies-other

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.

| S-ECPF-GEOD-44827 | biostudies-other

Gene expression analysis of pancreatic cancer associated fibroblasts

Project description:Gene expression analysis of pancreatic cancer associated fibroblasts and control fibroblasts To identify signaling pathways important in tumor-stromal cell interactions, we performed gene expression profiling on pancreatic cancer associated fibroblast cultures and control fibroblast cultures using Affymetrix Exon arrays. We analyzed 3 control fibroblast cultures and 9 pancreatic cancer associated fibroblast cultures using the Affymetrix Human Exon 1.0 ST platform. Gene expression levels were compared using Partek (version 6.3beta).

| S-ECPF-GEOD-21440 | biostudies-other

Gene expression profile analysis of ENO1 knockdown in gastric cancer cell line MGC-803.

Project description:Gastric cancer (GC) is the third leading cause of cancer-associated mortality. In a previous study, we identified that α-enolase (ENO1) promoted cell migration in GC, but the underlying molecular mechanisms remain to be fully elucidated. In the present study, small interfering RNAs were identified to interfere with ENO1 expression. The cDNA expression profiling was performed using an Affymetrix mRNA array platform to identify genes that may be associated with ENO1 in human GC cell line MGC-803. The differentially expressed genes (DEGs) were identified using the reverse transcription-quantitative polymerase chain reaction, followed by a series of bioinformatic analyses. As a result, there were 448 DEGs, among which 183 (40.85%) were downregulated. The most significant functional terms for the DEGs were the nuclear lumen for cell components (P=2.83×10-4), transcription for biological processes (P=3.7×10-7) and transcription factor activity for molecular functions (P=1.16×104). In total, six significant pathways were enriched, including the most common cancer-associated forkhead box O signaling pathway (P=0.0077), microRNAs in cancer (P=0.0183) and the cAMP signaling pathway (P=0.0415). Furthermore, a network analysis identified three hub genes (HUWE1, PPP1CB and HSPA4), which were all involved in tumor metastasis. Taken together, the DEGs, significant pathways and hub genes identified in the present study shed some light on the molecular mechanisms of ENO1 involved in the pathogenesis of GC.

| S-EPMC6425391 | biostudies-literature

Transcriptome analysis of pancreatic cancer cell line that differ in metastatic potential

Project description:Two pancreatic cancer cell lines with different metastatic and growth potential were compared under hypoxic conditions and under normal atmospheric oxygen pressure. The FG cell lines shows very few metastases and slow growth in mouse xenograft models. L3.6pl, derived from FG by cycles re-implantation of metastatic cells obtained after orthotopic tumor growth in nude mice, shows high motility, aggressive growth and very high metastatic potential By comparison of the two cell lines under different oxygen concentration we tried to simulate in vivo conditions of tumors at different growth stages. Differentially expressed genes and transcription factor regulating coexpressed genes identified by SOTA clustering were used to identify key genes that define metastatic potential of pancreatic cancer cells Keywords: 2+2 factorial design 12 samples, two cell lines * two culture conditions(oxygen pressure) * three replicates

| S-ECPF-GEOD-9350 | biostudies-other

Gene expression analysis of U251 human glioblastoma cell line

Project description:The human TP53 gene is frequently mutated in tumors and cell lines. Unlike other tumor suppressors that are commonly inactivated by deletions or nonsense mutations, the majority of p53-mutations are missense point mutations that result in the expression of a full-length protein with an altered amino acid that has lost sequence specific DNA-binding. Expression of mutant p53 (mutp53) confers advantages to tumor cells and transcriptional regulation of several genes mediating the beneficial effects has been shown to play a role. However, molecular mechanisms of transcriptional regulation by mutp53 are still poorly understood. We used the glioblastoma-derived U-251 MG human cell line endogenously expressing mutp53 protein (R273H mutation) to analyze gene expression profiles on Agilent Whole Human Genome Microarray after transient and stable depletion of mutp53 expression. Gene expression data was correlated with a ChIP study on a custom tiling array to understand the contribution of endogenously expressed mutp53 to transcriptional regulation. This series of microarray experiments contains the gene expression profiles of glioblastoma-derived U-251 MG human cell lines engineered to constitutively express a p53-specific shRNA or scrambled control shRNA. To reverse the effect of mutp53 depletion, stable clones were modified by stable integration of a mutp53-R273H expression construct or empty pCDNA3 vector as a control. In addition, we performed gene expression analysis of U-251 MG cells transiently transfected with p53-specific siRNA or control siRNA (3 biological replicates each).

| S-ECPF-GEOD-35454 | biostudies-other

Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling.

Project description:Recently, more and more studies show that long non-coding RNAs (lncRNAs) play a very important role in various biological processes. However, research on lncRNA in the tumor cell drug resistance of it is seldom reported. In this study, gemcitabine-resistant pancreatic cancer cell line SWl990/GZ was obtained by treating parental cell line SWl990 in vitro with increasing dosage of gemcitabine in culture medium intermittently for ten months. We identified 4983 of 13310 detected lncRNAs demonstrated > 2-fold abnormally expressed in response to the gemcitabine-resistant, among of them, 1993 and 2990 lncRNAs were upregulated and downregulated. Meanwhile, 4759 mRNAs exhibited at least a 2-fold, of these, 2671 and 2088 mRNAs were upregulated and downregulated. Gene Ontology analysis and Pathway analysis revealed that differential expression mRNA involved in significant biological regulatory function and some genes may be particular to pancreatic cancer chemotherapy resistance. Quantitative real time PCR confirmed the changes of six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) and nine mRNAs (SYT1, FAM171B, ZNF331, FAM187B, CYP1A1, SRXN1, HIST1H2BL, TOMM40L and SPP1) in SW1990 and SW1990/GZ. We also found that the upregulating of gemcitabine on the expression of lincRNA-ZNF532 was time-dependent. Gemcitabine at a range from 1.0 μM to 16.0 μM induced a increase of lincRNA-ZNF532 in SW1990 cells. The relative level of DDX6P is opposite to that of lincRNA-ZNF53 in the same circumstance. In conclusion, the dysregulated lncRNAs and mRNAs identified in this work may represent good candidates for future diagnostic or prognostic biomarkers and therapeutic targets.

| S-EPMC4348861 | biostudies-literature

Expression analysis of human pancreatic cancer cell lines (Capan-1, Panc-1, Panc-1+ve and Panc-1-ve) and pancreatic ductal cell line (HPDE)

Project description:Analysis of differentially expressing genes in whole genome wide analysis of aptamer SQ2 positive cells (Capan-1, Panc-1, Panc-1+ve) and SQ2 negative cells (Panc-1-ve and HPDE) Panc-1 +ve and Panc-1-ve cell lines were generated from Panc-1 cell line based upon its hetergenous binding to aptamer SQ2. Detailed procedure of generation of these cell lines are described in Pooja Dua, Hye Suk Kang, Seung-Mo Hong, Ming-Sound Tsao, Soyoun Kim, and Dong-ki Lee. 2012 Alkaline Phosphatase ALPPL2 is a novel pancreatic carcinoma-associated protein. Cancer Research A five chip study using total RNA recovered from Capan-1, Panc-1, Panc-1+ve, Panc-1-ve and HPDE cells. Each chip measures 45,033 genes with three 60 mer probe pairs per target.

| S-ECPF-GEOD-42428 | biostudies-other

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