Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma.

Aurora kinases B (AURKB), which plays a critical role in chromosomal segmentation and mitosis, greatly promotes cell cycle progression and aggressive proliferation of cancers. So far, its role and underlying mechanisms in mediating poor outcome of lung adenocarcinoma (LUAD) remained largely unclear. Analyses on multiple omics data of lung adenocarcinoma cohort in The Cancer Genome Atlas (TCGA) were performed based on AURKB expression, and demonstrated its association with clinical characteristics and the potential of using AURKB as a biomarker in predicting patients' survival. This study found aberrant alterations of genomics and epigenetics, including up-regulation and down-regulation of oncogenic genes and tumor suppressors, pathways involved in the cell cycle, DNA repair, spliceosome, and proteasome, hypermethylation enrichments around transcriptional start sites, which are all related to AURKB expression. We further discovered the possible role of tumor suppressors DLC1 and HLF in AURKB-mediated adverse outcome of LUAD. To conclude, this study proved AURKB as a potential prognostic factor and therapeutic target for lung adenocarcinoma treatment and provide a future research direction.