SRC and TP53 play critical role in low-grade dysplasia colorectal mucosa transformation into cancer.

Abstract

Determination of crucial genes that are involved in onset and progress of dysplasia of colorectal mucosa is the aim of this study. Management of dysplasia as one of the risk factors of colon cancer is very challenging. Molecular studies could be helpful in this matter. Here, the transcriptome profile of low-grade dysplasia in colon tissue in comparison with normal one is studied by protein-protein interaction (PPI) network analysis. For detecting differentially expressed genes (DEGs) of dysplasia lesion, the data was downloaded from the gene chip GSE31106, platform GPL1261, GSM770092-94 as normal colorectal mucosa group and GSM770098-100 as low-grade dysplasia colorectal mucosa from the Gene Expression Omnibus database (GEO). The expression profile is evaluated by GEO2R and a network of DEGs is constructed and analyzed by Cytoscape algorithms. The findings indicate that a PPI network analysis of 113 DEGs is consist of 8 nodes that 6 of them are common with inflammation state. Only SRC and TP53 were recognized as the specific makers for dysplasia. In this respect, a subnetwork of these two genes introduce a panel of 8 nodes consist of HRAS, MYC, PIK3CA, PIK3CB, PIK3CD, PIK3CG, SRC, and TP53. It can be concluded that SRC and TP53 may play prominent role in dysplasia pathogenicity after running validation tests.