Integrative multi-omics analysis reveals the landscape of Cyclin-Dependent Kinase (CDK) family genes in pan-cancer

Abstract Objective Cyclin-Dependent Kinases (CDKs) get widely involved in cancer development. However, A wealth of conflicting data raise the question of whether CDKs serve as oncogenes or cancer suppressors. Direct evidence from a same-batch cohort with matched multi-omics sequencing data is still lacking. Methods Here, we integrated multi-omics analysis to explore CDKs across multiple cancer types using data from The Cancer Genome Atlas (TCGA) database. First, we evaluated the expression levels of CDKs in pan-cancer. Second, we conducted copy number variants (CNV) and somatic mutation analysis of CDKs in pan-caner. Third, the biological functions of CDKs were obtained through pathway analysis. Finally, in order to explore effective drugs for tumors with obvious effects of CDKs, drug sensitivity analysis is also explored. Results To our surprise, CDKs are overexpressed in a wide range of cancers (39 upregulated, 12 downregulated cases), among which CDK1 is the top overexpressed gene (7 of 10 cancers). We next observed that CDK gene regions are heterozygously amplificated in cancer genomes. Further pathway analysis revealed that CDK genes cancer hallmarks such as apoptosis and cell cycle. CDK genes associate with 58 drug sensitivity including Trametinib and I-BET-762. Conclusions Taken together, our study identified a panel of clinically relevant CDK genes, defined the genomic/epigenomic/transcriptomic landscape of CDKs at a system level, and opened potential therapeutic opportunities for cancer patients.