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      Aurora Kinase B Inhibition: A Potential Therapeutic Strategy for Cancer

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          Abstract

          Aurora kinase B (AURKB) is a mitotic serine/threonine protein kinase that belongs to the aurora kinase family along with aurora kinase A (AURKA) and aurora kinase C (AURKC). AURKB is a member of the chromosomal passenger protein complex and plays a role in cell cycle progression. Deregulation of AURKB is observed in several tumors and its overexpression is frequently linked to tumor cell invasion, metastasis and drug resistance. AURKB has emerged as an attractive drug target leading to the development of small molecule inhibitors. This review summarizes recent findings pertaining to the role of AURKB in tumor development, therapy related drug resistance, and its inhibition as a potential therapeutic strategy for cancer. We discuss AURKB inhibitors that are in preclinical and clinical development and combination studies of AURKB inhibition with other therapeutic strategies.

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          GEPIA: a web server for cancer and normal gene expression profiling and interactive analyses

          Zefang Tang, Chenwei Li, Boxi Kang … (2017)
          Abstract Tremendous amount of RNA sequencing data have been produced by large consortium projects such as TCGA and GTEx, creating new opportunities for data mining and deeper understanding of gene functions. While certain existing web servers are valuable and widely used, many expression analysis functions needed by experimental biologists are still not adequately addressed by these tools. We introduce GEPIA (Gene Expression Profiling Interactive Analysis), a web-based tool to deliver fast and customizable functionalities based on TCGA and GTEx data. GEPIA provides key interactive and customizable functions including differential expression analysis, profiling plotting, correlation analysis, patient survival analysis, similar gene detection and dimensionality reduction analysis. The comprehensive expression analyses with simple clicking through GEPIA greatly facilitate data mining in wide research areas, scientific discussion and the therapeutic discovery process. GEPIA fills in the gap between cancer genomics big data and the delivery of integrated information to end users, thus helping unleash the value of the current data resources. GEPIA is available at http://gepia.cancer-pku.cn/.
          Article 0 comments Cited 3635 times – based on 0 reviews     Review now
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            Comprehensive analysis of kinase inhibitor selectivity.

            Mindy I Davis, Jeremy P Hunt, Sanna Herrgard … (2011)
            We tested the interaction of 72 kinase inhibitors with 442 kinases covering >80% of the human catalytic protein kinome. Our data show that, as a class, type II inhibitors are more selective than type I inhibitors, but that there are important exceptions to this trend. The data further illustrate that selective inhibitors have been developed against the majority of kinases targeted by the compounds tested. Analysis of the interaction patterns reveals a class of 'group-selective' inhibitors broadly active against a single subfamily of kinases, but selective outside that subfamily. The data set suggests compounds to use as tools to study kinases for which no dedicated inhibitors exist. It also provides a foundation for further exploring kinase inhibitor biology and toxicity, as well as for studying the structural basis of the observed interaction patterns. Our findings will help to realize the direct enabling potential of genomics for drug development and basic research about cellular signaling.
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              The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore–microtubule attachment and in maintaining the spindle assembly checkpoint

              Silke Hauf, Richard Cole, Sabrina LaTerra … (2003)
              The proper segregation of sister chromatids in mitosis depends on bipolar attachment of all chromosomes to the mitotic spindle. We have identified the small molecule Hesperadin as an inhibitor of chromosome alignment and segregation. Our data imply that Hesperadin causes this phenotype by inhibiting the function of the mitotic kinase Aurora B. Mammalian cells treated with Hesperadin enter anaphase in the presence of numerous monooriented chromosomes, many of which may have both sister kinetochores attached to one spindle pole (syntelic attachment). Hesperadin also causes cells arrested by taxol or monastrol to enter anaphase within <1 h, whereas cells in nocodazole stay arrested for 3–5 h. Together, our data suggest that Aurora B is required to generate unattached kinetochores on monooriented chromosomes, which in turn could promote bipolar attachment as well as maintain checkpoint signaling.
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                Author and article information

                Contributors
                Roberta Bortolozzi: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Molecules
                Journal ID (iso-abbrev): Molecules
                Journal ID (publisher-id): molecules
                Title: Molecules
                Publisher: MDPI
                ISSN (Electronic): 1420-3049
                Publication date (Electronic): 01 April 2021
                Publication date Collection: April 2021
                Volume: 26
                Issue: 7
                Electronic Location Identifier: 1981
                Affiliations
                [1 ]The Operation Eyesight Universal Institute for Eye Cancer, L.V. Prasad Eye Institute, Bhubaneswar 751024, India; naheed.borah@ 123456gmail.com
                [2 ]School of Biotechnology, KIIT University, Bhubaneswar 751024, India
                Author notes
                [* ]Correspondence: mamathamuppidi@ 123456gmail.com or mamatha@ 123456lvpei.org ; Tel.: +91-6743987175
                Author information
                https://orcid.org/0000-0003-0191-400X
                https://orcid.org/0000-0002-3492-4661
                Article
                Publisher ID: molecules-26-01981
                DOI: 10.3390/molecules26071981
                PMC ID: 8037052
                PubMed ID: 33915740
                SO-VID: 878cde2e-0c54-40c3-b1df-a9c6523e9e00
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 04 March 2021
                Date accepted : 23 March 2021
                Categories
                Subject: Review

                Keywords: aurora kinase b (aurkb),cancer,aurkb regulation,aurkb inhibitors,therapy related drug resistance,combination therapy
                Data availability:
                Keywords: aurora kinase b (aurkb), cancer, aurkb regulation, aurkb inhibitors, therapy related drug resistance, combination therapy

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