Pan-cancer investigation of CENPK gene: clinical significance and oncogenic immunology.

ABSTRACT

Many studies have confirmed that the CENPK gene regulates the progression of cancers, but its specific molecular mechanism remains unidentified, as does its significance in the analysis of human cancers. We specify a comprehensive genomic architecture of the CENPK gene associated with the tumor immune microenvironment and its clinical relevance across a broad spectrum of solid tumors. Statistics from The Cancer Genome Atlas (TCGA) and Cancer Cell Line Encyclopedia (CCLE) of over 30 solid tumors were examined. CENPK was expressed differentially in several cancers and is significantly associated in survival outcomes, with higher CENPK signifying a worse prognosis for ACC, KICH, KIRC, KIRP, LGG, LIHC, LUAD, MESO, and SARC. We further examined its clinical relevance with tumor immunogenic features. The expression level of CENPK was not only strongly linked to the tumor infiltration, such as tumor-infiltrating immune cells and immune scores but also linked to microsatellite instability and tumor mutation burden in diverse cancers (P<0.05). I mmune markers such as TNFRSF14 and VSIR were highly expressed on over 20 kinds of human cancer and mismatch repair genes like MLH1, MSH2, MSH6, and PMS2 were positively related with CENPK expression. Moreover, the methyltransferases and functional pathways also seem to have a relationship with the CENPK. CENPK is expected to be a guiding marker gene for clinical prognosis and tumor personalized immunotherapy.