Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

27 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of different gene expression levels in gastric cancer cell lines with drug treatment

ABSTRACT: A microarray time series was generated to identify which factor is expressed at different levels in two different gastric cancer cell lines, SNU 601 and SNU 668. These cell lines were treated for three different periods of time (24h, 48h, and 72h) with 1umol/L of olaparib or DMSO. Total RNA was extracted by using TRI reagent in accordance with the manufacturer`s instructions, and hybridized to an affymetrix GeneChip Human Gene 1.0 ST array. The results were normalized to the RObust Multi-Array Avarage (RMA) and analyzed.

ORGANISM(S): Homo sapiens

SUBMITTER: Ahrum Min

PROVIDER: E-MTAB-1012 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

RAD51C-deficient cancer cells are highly sensitive to the PARP inhibitor olaparib.

Min Ahrum A Im Seock-Ah SA Yoon Young-Kwang YK Song Sang-Hyun SH Nam Hyun-Jin HJ Hur Hyung-Seok HS Kim Hwang-Phill HP Lee Kyung-Hun KH Han Sae-Won SW Oh Do-Youn DY Kim Tae-You TY O'Connor Mark J MJ Kim Woo-Ho WH Bang Yung-Jue YJ

Molecular cancer therapeutics 20130319 6

A PARP inhibitor is a rationally designed targeted therapy for cancers with impaired DNA repair abilities. RAD51C is a paralog of RAD51 that has an important role in the DNA damage response. We found that cell lines sensitive to a novel oral PARP inhibitor, olaparib, had low levels of RAD51C expression using microarray analysis, and we therefore hypothesized that low expression of RAD51C may hamper the DNA repair process, resulting in increased sensitivity to olaparib. Compared with the cells wi ...[more]

PMID: 23512992

Similar Datasets

RNA transcriptome sequencing analysis of SNU-668 Erastin-resistant cells and SNU-668 parental cells, SNU-484 RSL3-resistant cells and SNU-484 parental cells

Project description:RNA transcriptome sequencing analysis was performed in SNU-668 Erastin-resistant cells and SNU-668 parental cells, SNU-484 RSL3-resistant cells and SNU-484 parental cells

2024-04-04 | GSE262114 | GEO

CG200745, an HDAC inhibitor, induces anti-tumour effects in cholangiocarcinoma cell lines targeting the Hippo pathway

Project description:The effects of CG200745 on SNU-1196 and SNU-1196/GR (gemcitabine resistant cell line) were assessed by cDNA and miRNA microarray analyses after 24 h of treatment.

2018-08-31 | E-MTAB-5733 | biostudies-arrayexpress

Microarray analysis of long noncoding RNAs in exosomes from SNU-668 Erastin-resistant cells and parental SNU-668 cells

Project description:a microarray analysis of long noncoding RNAs was performed in exosomes from SNU-668 Erastin-resistant cells and parental SNU-668 cells

2022-09-02 | GSE212303 | GEO

Human hepatocarcinoma cells : Huh-7 vs. SNU-739

Project description:Transcriptional profiling of human hepatocarcinoma comparing Huh-7 and SNU-739. Two-condition experiment, normalized ratio represented by Huh-7/SNU-739. Biological replicates: 2 Huh-7 replicates, 2 SNU-739 replicates.

2014-04-29 | E-GEOD-57106 | biostudies-arrayexpress

RNA transcriptome sequencing analysis of SNU-668 Erastin-resistant cells transfected with shRNA-SOX13 or control shRNA

Project description:a RNA transcriptome sequencing analysis was performed in SNU-668 erastin-resistant cells that were transfected with shRNA-SOX13 or control shRNA

2022-08-18 | GSE211072 | GEO

Role of SIRT1 in human hepatocellular carcinoma

Project description:To investigate the specific roles of SIRT1 in the development of hepatocellular carcinoma, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the SNU-182 cells transfected with SIRT1 siRNA and recapitulated molecular signatures that related to hallmarks of cancer. SIRT1 expression in hepatocellular carcinoma was analyzed by RT-PCR and western blot. RNA interference-mediated protein knockdown method was used to investigate oncogenic potential of SIRT1 in hepatocelluar carcinoma

2012-03-01 | E-GEOD-32066 | biostudies-arrayexpress

MET Amplified Gastric Cancer Cell Lines +/- Crizotinib

Project description:MET amplification is present in 20% of gastric cancers and has been confirmed as a therapeutic target in clinical trials. The molecular mechanisms of response and resistance to MET inhibitors are not well understood. We investigated the determinants of MET dependency in human gastric cancer. MET inhibition inhibited proliferation and induced cell death only in MET-amplified gastric cancer cell lines. The effects on growth arrest were stronger than the effects on cell death. To identify possible resistance mechanisms, we performed whole-genome mRNA expression profiling. Molecular changes related to autophagy were among the top alterations observed. Consistent with these findings, autophagy levels increased in a concentration-dependent manner when MET-amplified cells were exposed to crizotinib. Autophagy inhibition caused a dramatic decrease in apoptosis in one of the MET-amplified cell lines (MKN45) but not in the other (SNU-5). Because autophagy may provide energy in cells subjected to growth factor deprivation, we explored the effects of MET or autophagy inhibition on cellular ATP levels. This revealed that autophagy-dependent ATP production was selectively required for apoptosis in the MKN45 cells and that chemical ATP depletion mimicked the effects of autophagy inhibition to block cell death. Overall, the data reveal a novel relationship between ATP depletion and resistance to MET inhibitor-induced cell death. Our observations suggest that autophagy inhibitors could have unintended consequences when they are combined with growth factor receptor inhibitors in tumors that require autophagy-dependent ATP production for apoptosis. 12 samples triplicate samples of SNU-5 and MKN45 +/- criztonib for 24 hours

2016-05-13 | E-GEOD-77320 | biostudies-arrayexpress

A novel role of stem cell factor SALL4 as an oncofetal protein in hepatocellular carcinoma

Project description:Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. Treatment of HCC remains abysmal; discovery of novel pathways implicated in hepatocarcinogenesis is needed for more effective therapeutics. SALL4 is a stem cell factor essential for the maintenance of embryonic stem cell self-renewal properties and expressed in fetal liver, but silenced in normal adult liver. We observed that expression of SALL4 in murine liver in a transgenic model led to development of HCC. In humans, SALL4 is re-expressed as an oncofetal protein in a subgroup of HCC patients with unfavorable prognoses. Loss-of-function studies demonstrated that SALL4 is essential for human HCC cell survival and tumorigenicity. We demonstrated that a peptide can block the oncogenic function of SALL4 in HCC by modulating the PTEN/AKT pathway. Our findings reveal a novel role of SALL4 in HCC with important implications for understanding disease mechanisms and development of innovative therapeutics. Cultured cells from HCC cell line SNU-398 with scrambled or SALL4 shRNA knockdown were used for RNA extraction and hybridization on Affymetrix microarrays.

2012-02-22 | E-GEOD-35965 | biostudies-arrayexpress

Genome-wide analysis of enzalutamide- and/or olaparib-responsive gene expression in prostate cancer cells

Project description:Analysis of enzalutamide- and/or olaparib-responsive gene expression in prostate cancer cells. The hypothesis tested in the present study was that enzalutamide influences the expression of genes that are involved in important bioprocesses in prostate cance rcells, including DNA damage response genes and this effect may synergize with poly(ADP-ribose) polymerase inhibitor olaparib in cytotoxicity to prstate cancer cells. prostate cancer cells were pretreated with enzalutamide or vehicle control DMSO for 24 h, followed by treatment with enzalutamide, olaparib, enzalutamide+olaparib, or vehicle control DMSO for 48 h. Gene expression in enzalutamide+olaparib-treated cells was compared with taht in vehicle control- and single agent-treated cells.

2016-07-03 | E-GEOD-69249 | biostudies-arrayexpress

Identification of p53-regulated microRNAs in Hapatocellular Carcinoma (HCC).

Project description:p53 suppresses tumor progression and metastasis by regulating a large set of genes and microRNAs. By profiling 92 primary hepatocellular carcinomas (HCCs) and 9 HCC cell lines, we found that p53 upregulates microRNAs including miR-200 and miR-192 family members. By sequencing TP53 in 92 HCC samples, we classified the 92 samples into two groups (wt and mut). We also classified 9 HCC cell lines by testing p21 expression after DNA-damage mediated p53 activation. We then profiled microRNA expression in 92 HCC tissue samples and 9 HCC celll lines to identify p53-regulated microRNAs.

2011-05-11 | E-GEOD-28661 | 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