SRC and TP53 play critical role in low-grade dysplasia colorectal mucosa transformation into cancer
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Updated: Jan 29, 2026
Colorectal Cancer Cell Surface Protein Profiling Using an Antibody Microarray and Fluorescence Multiplexing
Published on: September 25, 2011
Hamid Asadzadeh-Aghdaei1, Mona Zamanian Azodi2, Reza Vafaee3
1Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Aim:
Determination of crucial genes that are involved in onset and progress of dysplasia of colorectal mucosa is the aim of this study.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
It can be concluded that SRC and TP53 may play prominent role in dysplasia pathogenicity after running validation tests.
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