Abstract
Kinesin superfamily member 2C (KIF2C) is an essential regulator of the cell cycle and its aberrant expression can promote tumor progression. However, the mechanism of KIF2C in pan-cancer is unclear.Data were obtained from public databases, including The Cancer Genome Atlas (TCGA), UALCAN, TIMER and CellMiner. The data came from public databases such as The Cancer Genome Atlas (TCGA), UALCAN, TIMER, and CellMiner. We analyzed the correlation of KIF2C with expression, prognosis, tumor mutation burden (TMB), microsatellite instability (MSI), mismatch repairs (MMR), immune infiltration and anticancer drug sensitivity by R language.KIF2C was highly expressed in several tumors and correlated with poor prognosis. KIF2C expression was significantly correlated with TMB, MSI, MMRs, and immune checkpoint genes, and with the level of immune cell infiltration such as tumor-associated macrophage (TAM), cancer-associated fibroblasts (CAFs), myeloid-derived suppressor cells (MDSCs) and Tregs. The GO and KEGG results suggest that KIF2C is involved in immune regulation in addition to cell cycle regulation.In addition, KIF2C is associated with DNA methylation, m6A modifications and m7G modifications. Our data suggest that KIF2C is a prognostic biomarker linked to immunosuppression, targeting KIF2C may improve the outcome of immunotherapy. Our findings indicate that KIF2C is a prognostic biomarker associated with immunosuppression, and that targeting KIF2C may improve the outcome of immunotherapy.