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Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies

Survivin is the smallest member of the inhibitor of apoptosis protein family, which has key roles in regulating cell division and inhibiting apoptosis by blocking caspase activation. Survivin is highly expressed in most human cancers, such as lung, pancreatic and breast cancers, relative to normal t...

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Detalles Bibliográficos
Autores principales: Chen, Xun, Duan, Ning, Zhang, Caiguo, Zhang, Wentao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747886/
https://www.ncbi.nlm.nih.gov/pubmed/26918045
http://dx.doi.org/10.7150/jca.13332
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author Chen, Xun
Duan, Ning
Zhang, Caiguo
Zhang, Wentao
author_facet Chen, Xun
Duan, Ning
Zhang, Caiguo
Zhang, Wentao
author_sort Chen, Xun
collection PubMed
description Survivin is the smallest member of the inhibitor of apoptosis protein family, which has key roles in regulating cell division and inhibiting apoptosis by blocking caspase activation. Survivin is highly expressed in most human cancers, such as lung, pancreatic and breast cancers, relative to normal tissues. Aberrant survivin expression is associated with tumor cell proliferation, progression, angiogenesis, therapeutic resistance, and poor prognosis. Studies on the underlying molecular mechanisms indicate that survivin is involved in the regulation of cytokinesis and cell cycle progression, as well as participates in a variety of signaling pathways such as the p53, Wnt, hypoxia, transforming growth factor, and Notch signaling pathways. In this review, recent progress in understanding the molecular basis of survivin is discussed. Therapeutic strategies targeting survivin in preclinical studies are also briefly summarized.
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spelling pubmed-47478862016-02-25 Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies Chen, Xun Duan, Ning Zhang, Caiguo Zhang, Wentao J Cancer Review Survivin is the smallest member of the inhibitor of apoptosis protein family, which has key roles in regulating cell division and inhibiting apoptosis by blocking caspase activation. Survivin is highly expressed in most human cancers, such as lung, pancreatic and breast cancers, relative to normal tissues. Aberrant survivin expression is associated with tumor cell proliferation, progression, angiogenesis, therapeutic resistance, and poor prognosis. Studies on the underlying molecular mechanisms indicate that survivin is involved in the regulation of cytokinesis and cell cycle progression, as well as participates in a variety of signaling pathways such as the p53, Wnt, hypoxia, transforming growth factor, and Notch signaling pathways. In this review, recent progress in understanding the molecular basis of survivin is discussed. Therapeutic strategies targeting survivin in preclinical studies are also briefly summarized. Ivyspring International Publisher 2016-01-10 /pmc/articles/PMC4747886/ /pubmed/26918045 http://dx.doi.org/10.7150/jca.13332 Text en © Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions.
spellingShingle Review
Chen, Xun
Duan, Ning
Zhang, Caiguo
Zhang, Wentao
Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies
title Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies
title_full Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies
title_fullStr Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies
title_full_unstemmed Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies
title_short Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies
title_sort survivin and tumorigenesis: molecular mechanisms and therapeutic strategies
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747886/
https://www.ncbi.nlm.nih.gov/pubmed/26918045
http://dx.doi.org/10.7150/jca.13332
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