J Cancer 2016; 7(3):314-323. doi:10.7150/jca.13332

Review

Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies

Xun Chen1,*, Ning Duan1,*, Caiguo Zhang2,✉, Wentao Zhang1,✉

1. Hong-Hui Hospital, Xi'an Jiaotong University, College of Medicine, Xi'an, Shaanxi, China, 710054
2. Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, CO, USA, 80045
* These authors contribute equally to this work.

Abstract

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.

Keywords: survivin, apoptosis, cell cycle, cancer, therapy

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Chen X, Duan N, Zhang C, Zhang W. Survivin and Tumorigenesis: Molecular Mechanisms and Therapeutic Strategies. J Cancer 2016; 7(3):314-323. doi:10.7150/jca.13332. Available from http://www.jcancer.org/v07p0314.htm