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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....
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7950220/ https://www.ncbi.nlm.nih.gov/pubmed/33612479 http://dx.doi.org/10.18632/aging.202517 |
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author | Huang, Jie Zhang, Qianyun Shen, Juan Chen, Xueqin Ma, Shenglin |
author_facet | Huang, Jie Zhang, Qianyun Shen, Juan Chen, Xueqin Ma, Shenglin |
author_sort | Huang, Jie |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7950220 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-79502202021-03-23 Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma Huang, Jie Zhang, Qianyun Shen, Juan Chen, Xueqin Ma, Shenglin Aging (Albany NY) Research Paper 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. Impact Journals 2021-02-17 /pmc/articles/PMC7950220/ /pubmed/33612479 http://dx.doi.org/10.18632/aging.202517 Text en Copyright: © 2021 Huang et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Huang, Jie Zhang, Qianyun Shen, Juan Chen, Xueqin Ma, Shenglin Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma |
title | Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma |
title_full | Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma |
title_fullStr | Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma |
title_full_unstemmed | Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma |
title_short | Multi-omics analysis identifies potential mechanisms of AURKB in mediating poor outcome of lung adenocarcinoma |
title_sort | multi-omics analysis identifies potential mechanisms of aurkb in mediating poor outcome of lung adenocarcinoma |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7950220/ https://www.ncbi.nlm.nih.gov/pubmed/33612479 http://dx.doi.org/10.18632/aging.202517 |
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