Aging
Navigate
Submit an Article
Research Paper|Volume 13, Issue 4|pp 5946—5966

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

Jie Huang1,2, Qianyun Zhang1,2, Juan Shen3, Xueqin Chen3, Shenglin Ma1,2
  • 1Nanjing Medical University, Nanjing, China
  • 2Department of Oncology, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou, China
  • 3Department of Oncology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou, China
Received: April 23, 2020Accepted: December 23, 2020Published: February 17, 2021
https://doi.org/10.18632/aging.202517

Copyright: © 2021 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.