Analyzing the molecular mechanism of the tissue specificity of gastrointestinal stromal tumors by using...

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. About 70% of GIST occur in the stomach, 20% in the small intestine and less than 10% in the esophagus. This study aimed to explore the difference of gene expression profile of GIST between different tumor sites.

Microarray data GSE8167 (accession number of the microarray data) were available from Gene Expression Omnibus (GEO) which included 23 gastric and 9 small intestine untreated GIST samples, and then the differentially expressed genes (DEGs) between these samples were identified using t-test. Furthermore, pathway enrichment analysis was performed to these DEGs and one protein-protein interaction network was constructed by STRING. Additionally, BioNet in R was used to establish a sub-network with false discovery rate < 0.001, and genes in this sub-network were further subjected to gene ontology (GO) and pathway analyses.

A total 730 genes were differentially expressed between gastric samples and small intestine samples, indicating the tissue specifity of GIST. Pathway analysis suggested these DEGs disturbed ECM-receptor interaction, gap junction and colorectal cancer. Moreover, some nodes (such as PLAT, VEGFC, PGF and CHD7) in the sub-network were significantly enriched in blood vessel development (p=4.58E-06), appendage development (p=9.54E-06) and skeletal system development (p=2.40E-04), respectively. Finally, several DEGs in the sub-network, including VEGFC and PGF, mainly affected pathways in cancer, focal adhesion, bladder cancer and cytokine-cytokine receptor interaction.

Our results suggest that molecular mechanisms of GIST originating in different site were different. Our findings are helpful for physicians and researchers to study the tissue specificity of GIST.