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Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies

Insulin-like growth factors (IGFs) are essential for growth and survival that suppress apoptosis and promote cell cycle progression, angiogenesis, and metastatic activities in various cancers. The IGFs actions are mediated through the IGF-1 receptor that is involved in cell transformation induced by...

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Autores principales: Brahmkhatri, Varsha P., Prasanna, Chinmayi, Atreya, Hanudatta S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383470/
https://www.ncbi.nlm.nih.gov/pubmed/25866791
http://dx.doi.org/10.1155/2015/538019
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author Brahmkhatri, Varsha P.
Prasanna, Chinmayi
Atreya, Hanudatta S.
author_facet Brahmkhatri, Varsha P.
Prasanna, Chinmayi
Atreya, Hanudatta S.
author_sort Brahmkhatri, Varsha P.
collection PubMed
description Insulin-like growth factors (IGFs) are essential for growth and survival that suppress apoptosis and promote cell cycle progression, angiogenesis, and metastatic activities in various cancers. The IGFs actions are mediated through the IGF-1 receptor that is involved in cell transformation induced by tumour. These effects depend on the bioavailability of IGFs, which is regulated by IGF binding proteins (IGFBPs). We describe here the role of the IGF system in cancer, proposing new strategies targeting this system. We have attempted to expand the general viewpoint on IGF-1R, its inhibitors, potential limitations of IGF-1R, antibodies and tyrosine kinase inhibitors, and IGFBP actions. This review discusses the emerging view that blocking IGF via IGFBP is a better option than blocking IGF receptors. This can lead to the development of novel cancer therapies.
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spelling pubmed-43834702015-04-12 Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies Brahmkhatri, Varsha P. Prasanna, Chinmayi Atreya, Hanudatta S. Biomed Res Int Review Article Insulin-like growth factors (IGFs) are essential for growth and survival that suppress apoptosis and promote cell cycle progression, angiogenesis, and metastatic activities in various cancers. The IGFs actions are mediated through the IGF-1 receptor that is involved in cell transformation induced by tumour. These effects depend on the bioavailability of IGFs, which is regulated by IGF binding proteins (IGFBPs). We describe here the role of the IGF system in cancer, proposing new strategies targeting this system. We have attempted to expand the general viewpoint on IGF-1R, its inhibitors, potential limitations of IGF-1R, antibodies and tyrosine kinase inhibitors, and IGFBP actions. This review discusses the emerging view that blocking IGF via IGFBP is a better option than blocking IGF receptors. This can lead to the development of novel cancer therapies. Hindawi Publishing Corporation 2015 2015-03-19 /pmc/articles/PMC4383470/ /pubmed/25866791 http://dx.doi.org/10.1155/2015/538019 Text en Copyright © 2015 Varsha P. Brahmkhatri et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Brahmkhatri, Varsha P.
Prasanna, Chinmayi
Atreya, Hanudatta S.
Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies
title Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies
title_full Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies
title_fullStr Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies
title_full_unstemmed Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies
title_short Insulin-Like Growth Factor System in Cancer: Novel Targeted Therapies
title_sort insulin-like growth factor system in cancer: novel targeted therapies
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383470/
https://www.ncbi.nlm.nih.gov/pubmed/25866791
http://dx.doi.org/10.1155/2015/538019
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