Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

66 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 or overexpression of SNHG5

ABSTRACT: Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5 A four chip study using total RNA extracted from SGC-7901 cells transfected with siRNA negative control and SGC-7901 cells knock down of MTA2 with siRNA. Each chip measures the expression level of 45033 genes collected from the authoritative data source including NCBI

ORGANISM(S): Homo sapiens

SUBMITTER: Shi Juan

PROVIDER: E-GEOD-65915 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression analysis of gastric carcinoma tissues and cell line SGC-7901

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

2015-09-09 | E-GEOD-65917 | biostudies-arrayexpress

Expression analysis of gastric cancer cells treated with periplocin

Project description:To further analyze the change of differential gene expression between SGC-7901 cells treated with 100ng/ml periplocin and untreated cells, respectively. We employed whole genome microarray expression profiling as a discovery platform to identify genes. Gene expression in SGC-7901 cells treated with 100ng/ml periplocin for 24h at 37 ÂºC in a humidified incubator with 5% CO2.

2016-02-23 | E-GEOD-78211 | biostudies-arrayexpress

Expression profiling on HPSE deleted SGC-7901 gastric cancer cells

Project description:HPSE plays important roles in gastric cancer cell proliferation, apoptosis and metastasis.The aim of this study is to explore molecular mechanism underling roles of HPSE in gastric cancer cell proliferation, survival, migration and metastasis. SGC-7901 gastric cancer cells were transfected with HPSE siRNA (10nM) or scramble control siRNA, RNA were extracted 24hours after transfectioin and hybridized to Affymetrix microarrays. 3 biological repeats were used for each condition.

2013-12-02 | E-GEOD-34080 | biostudies-arrayexpress

Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 or overexpression of SNHG5

Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5

2015-09-09 | GSE65915 | GEO

Differential gene expression between BGC-823/NC and BGC-823/MTA2, SGC-7901/NC and SGC-7901/shMTA2 cells

Project description:Metastasis associated 1 family, member 2 (MTA2) gene is classified to metastasis associated gene family. We have previously reported that MTA2 gene was overexpressed in gastric cancer tissues, correlating with tumor invasion, lymph node metastasis, and advanced TNM stage. MTA2 knockdown significantly inhibited gastric cancer cell invasion and metastasis. Yet, its molecular mechanisms are still unclear. The aim of this study is to investigate the molecular mechanisms of MTA2 in regulating malignant behaviors of gastric cancer. This experiment captures the expression data between BGC-823/NC and BGC-823/MTA2, SGC-7901/NC and SGC-7901/shMTA2 cells using Whole human genome microarray 4×44K (Design ID: 014850, Agilent technologies).

2015-04-08 | E-MTAB-3469 | biostudies-arrayexpress

Transcriptomic analysis of gastric cancer SGC-7901 cells in response to stable over-expression of intelectin 1

Project description:Gastric cancer is one of the most common cancers worldwide, with approximately 1 million patients being diagnosed annually. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of gastric cancer. Since our previous studies indicate that intelectin 1 (ITLN1) is aberrantly expressed in gastric cancer and serves as a prognostic factor for predicting the outcomes of gastric cancer patients, we hypothesized that ITLN1 might participate in the progression and aggressiveness of gastric cancer. We employed the human whole genome microarray expression profiling as a discovery platform to analyze the transcriptome profiling changes of human gastric cancer SGC-7901 cells in response to stable over-expression of ITLN1. The results showed that stable over-expression of ITLN1 led to altered expression of 1592 human mRNAs, including 547 up-regulated genes and 1045 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the microarray results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to ITLN1 over-expression in human gastric cancer cells, and these findings will help us understand the pathogenesis of gastric cancer. Total RNA of cells stably transfected with empty vector or ITLN1 was extracted using the TRIZOL Reagent according to the manufacturer's instructions. Gene expression profiling was performed for each RNA sample separately on the Agilent Whole Human Genome Oligo Microarray 4×44K at Shanghai Technology Corporation (Shanghai, China), in which GeneChip microarray service was certificated by Agilent.

2015-07-01 | E-GEOD-58962 | biostudies-arrayexpress

RNA-sequencing of SGC-7901 cells with and without PUM1 knockdown

Project description:In order to explore the effect of RNA-binding protein PUM1 on proliferation, metastasis and metabolism of gastric cancer, we established PUM1 stable knockdown SGC-7901 cell lines. We then performed gene expression profiling analysis using data obtained from RNA-seq of PUM1-knockdown and negative control SGC-7901 cells.

2022-09-10 | GSE212848 | GEO

RNA transcriptome sequencing analysis of SGC-7901 cells transfected with ENST00000431060 shRNA or control shRNA

Project description:RNA transcriptome sequencing analysis was performed in SGC-7901 cells that were transfected with ENST00000431060 shRNA or control shRNA

2018-10-02 | GSE112586 | GEO

Proteomic analysis in S100A16-overexpressed human gastric cancer cells lines

Project description:Our studies reveal that S100A16 overexpression triggers GC cells proliferation and migration both in vivo and in vitro; by contrast, S100A16 knockdown restricts the speed of GC cells growth and mobility. Proteomic analysis results reveal a large S100A16 interactome, which includes ZO-2 (Zonula Occludens-2), a master regulator of cell-to-cell tight junction

2022-02-17 | PXD028022 | Pride

Proteomic analysis of cell cycle arrest and differentiation induction caused by ATPR, a derivative of all-trans retinoic acid, in human gastric cancer SGC-7901 cells

Project description:Experimental design: Peptides digested from the total cellular proteins were analyzed by reverse phase LC–MS/MS followed by a label-free quantification analysis. The SEQUEST search engine was used to identify proteins and bioinformatics resources were used to investigate the involved pathways for the differentially expressed proteins. Results: 13 down-regulated proteins were identified in the ATPR-treated group. Bioinformatics analysis showed that the effects of ATPR on 14-3-3 might potentially involve the PI3K-AKT-FOXO pathway and P27Kip1 expression. Western blot and RT-PCR analysis showed that ATPR could inhibit AKT phosphorylation, up-regulate the expression of FOXO1A and P27Kip1 at both the protein and mRNA levels, and down-regulate the cytoplasmic expression of cyclin E and CDK2. ATPR-induced G0/G1 phase arrest and differentiation can be ablated if the P27kip1 gene is silenced with sequence-specific siRNA. Conclusions and clinical relevance: ATPR might cause cell cycle arrest and differentiation in SGC-7901 cells by simultaneously inhibiting the phosphorylation of AKT and down-regulating 14-3-3. This change would then enhance the inhibition of cyclin E/CDK2 by up-regulating FOXO1A and P27Kip1. Our findings could be of value for finding new drug targets and for developing more effective differentiation inducer.

2017-02-13 | PXD005605 | Pride

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