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Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases

SIMPLE SUMMARY: Lung cancer has remained one of the major causes of death worldwide. Thus, a more effective treatment approach is essential, such as the inhibition of specific cancer-promoting molecules. Aurora kinases regulate the process of mitosis—a process of cell division that is necessary for...

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Autores principales: Galetta, Domenico, Cortes-Dericks, Lourdes
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7697457/
https://www.ncbi.nlm.nih.gov/pubmed/33202573
http://dx.doi.org/10.3390/cancers12113371
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author Galetta, Domenico
Cortes-Dericks, Lourdes
author_facet Galetta, Domenico
Cortes-Dericks, Lourdes
author_sort Galetta, Domenico
collection PubMed
description SIMPLE SUMMARY: Lung cancer has remained one of the major causes of death worldwide. Thus, a more effective treatment approach is essential, such as the inhibition of specific cancer-promoting molecules. Aurora kinases regulate the process of mitosis—a process of cell division that is necessary for normal cell proliferation. Dysfunction of these kinases can contribute to cancer formation. In this review, we present studies indicating the implication of Aurora kinases in tumor formation, drug resistance, and disease prognosis. The effectivity of using Aurora kinase inhibitors in the pre-clinical and clinical investigations has proven their therapeutic potential in the setting of lung cancer. This work may provide further information to broaden the development of anticancer drugs and, thus, improve the conventional lung cancer management. ABSTRACT: Despite tremendous efforts to improve the treatment of lung cancer, prognosis still remains poor; hence, the search for efficacious therapeutic option remains a prime concern in lung cancer research. Cell cycle regulation including mitosis has emerged as an important target for cancer management. Novel pharmacological agents blocking the activities of regulatory molecules that control the functional aspects of mitosis such as Aurora kinases are now being investigated. The Aurora kinases, Aurora-A (AURKA), and Aurora B (AURKB) are overexpressed in many tumor entities such as lung cancer that correlate with poor survival, whereby their inhibition, in most cases, enhances the efficacy of chemo-and radiotherapies, indicating their implication in cancer therapy. The current knowledge on Aurora kinase inhibitors has increasingly shown high potential in ensuing targeted therapies in lung malignancies. In this review, we will briefly describe the biology of Aurora kinases, highlight their oncogenic roles in the pre-clinical and clinical studies in lung cancer and, finally, address the challenges and potentials of Aurora kinases to improve the therapy of this malignancy.
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spelling pubmed-76974572020-11-29 Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases Galetta, Domenico Cortes-Dericks, Lourdes Cancers (Basel) Review SIMPLE SUMMARY: Lung cancer has remained one of the major causes of death worldwide. Thus, a more effective treatment approach is essential, such as the inhibition of specific cancer-promoting molecules. Aurora kinases regulate the process of mitosis—a process of cell division that is necessary for normal cell proliferation. Dysfunction of these kinases can contribute to cancer formation. In this review, we present studies indicating the implication of Aurora kinases in tumor formation, drug resistance, and disease prognosis. The effectivity of using Aurora kinase inhibitors in the pre-clinical and clinical investigations has proven their therapeutic potential in the setting of lung cancer. This work may provide further information to broaden the development of anticancer drugs and, thus, improve the conventional lung cancer management. ABSTRACT: Despite tremendous efforts to improve the treatment of lung cancer, prognosis still remains poor; hence, the search for efficacious therapeutic option remains a prime concern in lung cancer research. Cell cycle regulation including mitosis has emerged as an important target for cancer management. Novel pharmacological agents blocking the activities of regulatory molecules that control the functional aspects of mitosis such as Aurora kinases are now being investigated. The Aurora kinases, Aurora-A (AURKA), and Aurora B (AURKB) are overexpressed in many tumor entities such as lung cancer that correlate with poor survival, whereby their inhibition, in most cases, enhances the efficacy of chemo-and radiotherapies, indicating their implication in cancer therapy. The current knowledge on Aurora kinase inhibitors has increasingly shown high potential in ensuing targeted therapies in lung malignancies. In this review, we will briefly describe the biology of Aurora kinases, highlight their oncogenic roles in the pre-clinical and clinical studies in lung cancer and, finally, address the challenges and potentials of Aurora kinases to improve the therapy of this malignancy. MDPI 2020-11-14 /pmc/articles/PMC7697457/ /pubmed/33202573 http://dx.doi.org/10.3390/cancers12113371 Text en © 2020 by the authors. 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/).
spellingShingle Review
Galetta, Domenico
Cortes-Dericks, Lourdes
Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases
title Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases
title_full Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases
title_fullStr Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases
title_full_unstemmed Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases
title_short Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases
title_sort promising therapy in lung cancer: spotlight on aurora kinases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7697457/
https://www.ncbi.nlm.nih.gov/pubmed/33202573
http://dx.doi.org/10.3390/cancers12113371
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