Abstract
BACKGROUND: There are often subtle early symptoms of colorectal cancer, a common malignancy of the intestinal tract. However, it is not yet clear how MYC and NCAPG2 are involved in colorectal cancer. METHOD: We obtained colorectal cancer datasets GSE32323 and GSE113513 from the Gene Expression Omnibus (GEO). After downloading, we identified differentially expressed genes (DEGs) and performed Weighted Gene Co-expression Network Analysis (WGCNA). We then undertook functional enrichment assay, gene set enrichment assay (GSEA) and immune infiltration assay. Protein-protein interaction (PPI) network construction and analysis were undertaken. Survival analysis and Comparative Toxicogenomics Database (CTD) analysis were conducted. A gene expression heat map was generated. We used TargetScan to identify miRNAs that are regulators of DEGs. RESULTS: 1117 DEGs were identified. Their predominant enrichment in activities like the cellular phase of the cell cycle, in cell proliferation, in nuclear and cytoplasmic localisation and in binding to protein-containing complexes was revealed by Gene Ontology (GO). When the enrichment data from GSE32323 and GSE113513 colon cancer datasets were merged, the primary enriched DEGs were linked to the cell cycle, protein complex, cell cycle control, calcium signalling and P53 signalling pathways. In particular, MYC, MAD2L1, CENPF, UBE2C, NUF2 and NCAPG2 were identified as highly expressed in colorectal cancer samples. Comparative Toxicogenomics Database (CTD) demonstrated that the core genes were implicated in the following processes: colorectal neoplasia, tumour cell transformation, inflammation and necrosis. CONCLUSIONS: High MYC and NCAPG2 expression has been observed in colorectal cancer, and increased MYC and NCAPG2 expression correlates with worse prognosis.