Abstract
BACKGROUND Gastric cancer (GC) is a worldwide malignancy and the molecular mechanism of the GC carcinogenesis has not been fully elucidated. Our previous study suggested CDCA5 played a role in GC development via regulating cell proliferation, migration, and apoptosis in GC cells. MATERIAL AND METHODS Here, we first carried out bioinformatics analysis and found cyclin-dependent kinase 1 (CDK1) was possibly associated with CDCA5 using STRING. Then, the expression levels of CDK1 and CDCA5 in cancer tissues were estimated through Oncomine and The Cancer Genome Atlas (TCGA) database. After that, functional experiments were exerted to detect the association of CDK1 and CDCA5. Finally, cell proliferation assay, colon formation assay, cell scratch assay, transwell migration and invasion assays were applied to explore the roles of CDK1 and CDCA5 in GC cells MGC-803. RESULTS CDK1 and CDCA5 were both upregulated and co-expressed in GC tissues. The expression of CDK1 and CDCA5 in MGC-803 was positively related. CDK1 or CDCA5 inhibition can suppress the proliferation, colon formation, migration, and invasion abilities of GC cells. CONCLUSIONS Co-expression of CDK1 and CDCA5 might confer cell proliferation, migration, and invasion abilities in GC cells, and this can provide some clues for further therapies of gastric tumors.