Background: This study systematically evaluated the expression profile and functional significance of minichromosome maintenance 10 (MCM10) in colorectal cancer (CRC), assessed its association with the tumor immune microenvironment, and investigated its role in regulating cellular proliferation, migration, invasion, and stemness, thereby highlighting its potential as a therapeutic candidate.

Methods: Transcriptomic datasets were accessed from publicly available databases (GEO and TCGA). The data were analyzed to determine MCM10 expression and assess its association with immune cell infiltration. Functional enrichment profiling and molecular network modeling were performed to uncover underlying mechanisms. Furthermore, in vitro validation, including quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) proliferation assays, Transwell migration and invasion assays, and tumor sphere formation assays, was conducted to determine the biological effects of MCM10 on CRC cells.

Results: MCM10 was upregulated in CRC tissues and demonstrated a positive association with immune-cell infiltration, particularly helper T cells and T helper 2 (Th2) cells. Notably, MCM10 expression was substantially higher in CRC tissues compared with adjacent normal tissues (p < 0.001), consistent with TCGA and GTEx cohort analyses. Furthermore, MCM10 was enriched in cancer-related signaling pathways and immune regulatory processes. Functional assays demonstrated that MCM10 overexpression promoted CRC cell proliferation, migration, invasion, and stemness, while its knockdown produced the opposite effects.

Conclusion: Our findings confirm a pivotal role of MCM10 in CRC, suggesting its potential as a diagnostic biomarker and therapeutic target. The findings offer promising insights into the molecular biology of CRC and provide a foundation for the development of precision treatment strategies.