Colorectal cancer (CRC) is one of the most prevalent diseases worldwide; however, the molecular mechanisms involved in CRC remain unclear. Thus, we aimed to explore a novel biomarker for CRC. In this study, we screened 361 differentially expressed genes; 152 downregulated genes; and 209 upregulated genes) through analysis of the GSE44861, GSE110223, GSE110224, and GSE113513 CRC datasets. Next, ASPM, CCNA2, CCNB1, CEP55, KIF20A, MAD2L1, MELK, RRM2, TOP2A, TPX2, TRIP13, and TTK were identified as hub genes associated with the cell cycle in CRC through comprehensive bioinformatics analysis using the Cytoscape and Metascape software, the Database for Annotation, Visualization, and Integrated Discovery (DAVID), and the Oncomine and Gene Expression Profiling Interactive Analysis 2 (GEPIA2) databases. Furthermore, ASPM mRNA expression in CRC tissues was verified in Oncomine, The Cancer Genome Atlas and our data, and ASPM was found to be significantly upregulated in CRC tissues compared with that in the noncancer colon tissues. Functionally, we showed that overexpression of ASPM significantly promoted the proliferation and inhibited apoptosis; silencing of ASPM suppressed the proliferation of CRC cells by affecting the cell cycle G1/S transition by reducing cyclin E1 expression, and inducing apoptosis. Overall, our findings indicated that ASPM plays a crucial role in the regulation of CRC cell proliferation, and ASPM is a potential candidate diagnostic tool and therapeutic target for CRC.
Keywords: ASPM; bioinformatics; colorectal cancer; proliferation.