Research Paper Volume 13, Issue 4 pp 5946—5966
Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma
- 1 Nanjing Medical University, Nanjing, China
- 2 Department of Oncology, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou, China
- 3 Department 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, 2020 Accepted: December 23, 2020 Published: February 17, 2021https://doi.org/10.18632/aging.202517
How to Cite
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.
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.
AURKA: Aurora Kinases A; AURKB: Aurora Kinases B; CDCA3: Cell Division Cycle Associated 3; CSF-1R: Colony Stimulating Factor 1 Receptor; CXCL12: C-X-C Motif Chemokine Ligand 12; CXCR4: C-X-C Motif Chemokine Receptor 4; DEG: Differentially Expressed Genes; DMR: Differentially Methylated Regions; DLC1: Deleted In Liver Cancer 1 Protein; E2F2: E2F Transcription Factor 2; EGFR: Epidermal Growth Factor Receptor; FAM64A: Family With Sequence Similarity 64 Member A; FDR: false discovery rate; GEO: Gene Expression Omnibus; GINS4: GINS Complex Subunit 4; GSEA: Gene Set Enrichment Analysis; HLF: Hepatic Leukemia Factor; HMGA2: High Mobility Group AT-Hook 2; KIF14: Kinesin Family Member 14; KIF23: Kinesin Family Member 23; KRAS: Kirsten Rat Sarcoma Viral Oncogene Homolog; LCE: Lung Cancer Explorer; LYPD6: LY6/PLAUR Domain Containing 6; MALAT-1: Metastasis Associated Lung Adenocarcinoma Transcript 1; NSCLC: Non-Small Cell Lung Cancer; OS: overall survival; PD1/PDL1: Programmed Death 1/Programmed Death-Ligand 1; PFS: progression-free survival; POLQ: DNA Polymerase Theta; PRAME: Preferentially Expressed Antigen in Melanoma; PRR11: Proline-Rich 11; TCGA: The Cancer Genomics Atlas; TKI: Tyrosine Kinase Inhibitor; TSS: Transcription Start Site; RAB3B: Ras-related Protein Rab-3B; WNK3: WNK Lysine Deficient Protein Kinase 3.