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Telomere length regulation through epidermal growth factor receptor signaling in cancer

Length of the telomere (TL), a structure at the tip of chromosome that protects and ensures stability, is determined by multi-protein complexes such as telosome/shelterin and telomerase. Earlier studies from our laboratory show that longer TL has potential to be positive predictive biomarker of clin...

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Detalles Bibliográficos
Autores principales: Augustine, Titto, Maitra, Radhashree, Goel, Sanjay
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5511888/
https://www.ncbi.nlm.nih.gov/pubmed/28740573
http://dx.doi.org/10.18632/genesandcancer.140
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author Augustine, Titto
Maitra, Radhashree
Goel, Sanjay
author_facet Augustine, Titto
Maitra, Radhashree
Goel, Sanjay
author_sort Augustine, Titto
collection PubMed
description Length of the telomere (TL), a structure at the tip of chromosome that protects and ensures stability, is determined by multi-protein complexes such as telosome/shelterin and telomerase. Earlier studies from our laboratory show that longer TL has potential to be positive predictive biomarker of clinical outcome to anti-epidermal growth factor receptor (EGFR) monoclonal antibody therapy in patients with KRAS WT metastatic colorectal cancer. Although there is extensive literature suggesting the role of shelterin and telomerase, not much literature exists that describes the role of EGFR and KRAS pathway in regulating TL. This detailed review focuses on an insight into various components, including proteins, enzymes and transcription factors, interlinking between EGFR pathways and telomerase that regulate TL.
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spelling pubmed-55118882017-07-24 Telomere length regulation through epidermal growth factor receptor signaling in cancer Augustine, Titto Maitra, Radhashree Goel, Sanjay Genes Cancer Review Length of the telomere (TL), a structure at the tip of chromosome that protects and ensures stability, is determined by multi-protein complexes such as telosome/shelterin and telomerase. Earlier studies from our laboratory show that longer TL has potential to be positive predictive biomarker of clinical outcome to anti-epidermal growth factor receptor (EGFR) monoclonal antibody therapy in patients with KRAS WT metastatic colorectal cancer. Although there is extensive literature suggesting the role of shelterin and telomerase, not much literature exists that describes the role of EGFR and KRAS pathway in regulating TL. This detailed review focuses on an insight into various components, including proteins, enzymes and transcription factors, interlinking between EGFR pathways and telomerase that regulate TL. Impact Journals LLC 2017-05 /pmc/articles/PMC5511888/ /pubmed/28740573 http://dx.doi.org/10.18632/genesandcancer.140 Text en Copyright: © 2017 Augustine et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Review
Augustine, Titto
Maitra, Radhashree
Goel, Sanjay
Telomere length regulation through epidermal growth factor receptor signaling in cancer
title Telomere length regulation through epidermal growth factor receptor signaling in cancer
title_full Telomere length regulation through epidermal growth factor receptor signaling in cancer
title_fullStr Telomere length regulation through epidermal growth factor receptor signaling in cancer
title_full_unstemmed Telomere length regulation through epidermal growth factor receptor signaling in cancer
title_short Telomere length regulation through epidermal growth factor receptor signaling in cancer
title_sort telomere length regulation through epidermal growth factor receptor signaling in cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5511888/
https://www.ncbi.nlm.nih.gov/pubmed/28740573
http://dx.doi.org/10.18632/genesandcancer.140
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