Published online Jan 26, 2015. doi: 10.4252/wjsc.v7.i1.208
Peer-review started: July 19, 2014
First decision: September 4, 2014
Revised: September 18, 2014
Accepted: November 17, 2014
Article in press: December 16, 2014
Published online: January 26, 2015
Processing time: 179 Days and 19.2 Hours
AIM: To investigate the genes regulated in mesenchymal stem cells (MSCs) and diffuse-type gastric cancer (GC), gene expression was analyzed.
METHODS: Gene expression of MSCs and diffuse-type GC cells were analyzed by microarray. Genes related to stem cells, cancer and the epithelial-mesenchymal transition (EMT) were extracted from human gene lists using Gene Ontology and reference information. Gene panels were generated, and messenger RNA gene expression in MSCs and diffuse-type GC cells was analyzed. Cluster analysis was performed using the NCSS software.
RESULTS: The gene expression of regulator of G-protein signaling 1 (RGS1) was up-regulated in diffuse-type GC cells compared with MSCs. A panel of stem-cell related genes and genes involved in cancer or the EMT were examined. Stem-cell related genes, such as growth arrest-specific 6, musashi RNA-binding protein 2 and hairy and enhancer of split 1 (Drosophila), NOTCH family genes and Notch ligands, such as delta-like 1 (Drosophila) and Jagged 2, were regulated.
CONCLUSION: Expression of RGS1 is up-regulated, and genes related to stem cells and NOTCH signaling are altered in diffuse-type GC compared with MSCs.
Core tip: Recent studies have revealed that epithelial-mesenchymal transition (EMT) regulators play important roles in cellular phenotypes. This study has shown that EMT-related genes are regulated in diffuse-type gastric cancer and mesenchymal stem cells (MSCs). Regulator of G-protein signaling 1 (RGS1) was significantly up-regulated in diffuse-type GC compared with MSCs. These results are interesting and provide insights about the mechanisms of the stem cell phenotype transition and gastric cancer progression. These insights will examine the novel role of EMT-related genes and RGS1.