Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Periplocymarin on Gene Expression in Gastric Cancer Cell Lines HGC27 and MKN45

ABSTRACT: Effect of Periplocymarin on Gene Expression in Gastric Cancer Cell Lines HGC27 and MKN45

PROVIDER: PRJNA1223184 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Effect of Periplocymarin on Gene Expression in Gastric Cancer Cell Lines HGC27 and MKN45

Project description:Periplocymarin (PPM) is an extract isolated from the traditional plant Periploca sepium with a cardiac glycoside-like structure. Previous studies have gradually revealed the anticancer potential of PPM. PPM exhibits a stronger inhibitory effect on tumor cell viability compared to ouabain, and it can both induce and sensitize TRAIL-induced apoptosis in cancer cells, while showing relatively low toxicity to PBMCs. The anticancer effects of PPM are influenced by several cellular processes it induces, such as autophagy and metabolism, although the exact mechanisms remain unclear. We have observed that PPM inhibits cell viability, proliferation, and the cell cycle in gastric cancer cells, but the process of inducing apoptosis in gastric cancer cells is moderate and slow. Therefore, there is an urgent need to elucidate the changes in the gene expression profile of tumor cells following PPM treatment, to better understand how PPM affects cellular biological processes and signaling pathways, thus maximizing its anticancer potential.

2025-02-18 | GSE289470 | GEO

Gene expression profile of HGC27 gastric cancer cell p53 KO and KD

Project description:HGC27 gastric cancer cells were manipulated to express mutant p53

2019-06-07 | GSE132333 | GEO

Expression data from human stomach cell lines (MKN45 and MKN45P)

Project description:Analysis to find splicing variants that are differentially expressed in a highly metastatic stomach cancer cell line, MKN45P, versus its parental cell line, MKN45 Comparison between highly metastatic gastric cancer cell line MKN45P and its parental cell line MKN45

2010-06-08 | E-GEOD-21572 | biostudies-arrayexpress

Affymetrix miRNA chip showed the differential miRNA expression in TRAIL‐resistant BGC823 and TRAIL‐sensitive MKN45 cells

Project description:In order to explore the effect of miRNA on TRAIL sensitivity of gastric cancer, we selected TRAIL-sensitive MKN45 and TRAIL-resistant BGC823 gastric cancer cell line. The expression of miRNA in MKN45 and BGC823 was detected by miRNA chip. "3" is the miRNA expression file of BGC823. "4" is the miRNA expression file of MKN45.

2020-05-24 | E-MTAB-9151 | biostudies-arrayexpress

Human gastric cancer cell MKN45: MKN45-GFP control vs. highly metastatic sublines

2011-11-10 | GSE33570 | GEO

Human gastric cancer cell MKN45: MKN45-GFP control vs. highly metastatic sublines

Project description:Gene expression profiles of in vitro selected highly metastatic MKN45-GFP sublines. The results were compared with MKN45-GFP control cell line to determine the metastasis associated genes. Four pairs compared experiment. Each pair was used MKN45-GFP cells as correlated control. Determining on the gene expression trends were by various metastatic ability of each subline.

2011-11-10 | E-GEOD-33570 | biostudies-arrayexpress

Genome-wide loop structure analysis in HGC27 gastric cancer cell.

Project description:We analysed loop structure between gene promoters and enhancers in HGC27 cell using H3K27ac HiChIP.

2025-03-04 | GSE198689 | GEO

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

Genome-wide loop structure analysis in HGC27 gastric cancer cell.

Project description:Genome-wide loop structure analysis in HGC27 gastric cancer cell.

| PRJNA816469 | ENA

Anti-proliferation activity of fucoidan on MKN45 gastric cancer cells and downregulation of phosphorylated ASK1, a cell-cycle-regulated cyclin-dependent kinase

Project description:Fucoidan is a high-molecular polysaccharide whose main constituent is sulfated fucose. Extensive studies have demonstrated numerous interesting biological activities for fucoidan. We specifically focused on the anti-proliferation activity of fucoidan and examined the underlying mechanism in MKN45 gastric cancer cells. BrdU assay revealed that fucoidan impeded the MKN45 cell cycle by approximately 50%, and clonogenic assay also showed that fucoidan inhibited cell proliferation. Preliminary examinations of fucoidan using LDH assay showed no immediate cytotoxic effects at 24-h exposure. However, longer time courses revealed inhibition of cell growth at 4 days in a dose-dependent manner. Microarray analysis in MKN45 cells treated with fucoidan identified genes that were upregulated and downregulated in response to fucoidan, including MAP3K5, or ASK1 (apoptosis signal-regulating kinase), which was upregulated by 1.38-fold. Western blot confirmed that fucoidan increased ASK1 protein levels, while reducing the levels of phosphorylated ASK1. Reduction of ASK1 by siRNA decreased proliferation of MKN45 cells. Our findings show that fucoidan may suppress cellular proliferation and DNA synthesis in MKN45 cells by suppressing the ASK1-p38 signaling pathway through reduction of phosphorylated ASK1 levels.

2017-02-09 | GSE58774 | GEO

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