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Trace of survivin in cancer

Shojaei, Fereshteha; Yazdani-Nafchi, Farshada; Banitalebi-Dehkordi, Mehdia; Chehelgerdi, Mohammada; Khorramian-Ghahfarokhi, Miladb

European Journal of Cancer Prevention: July 2019 - Volume 28 - Issue 4 - p 365–372
doi: 10.1097/CEJ.0000000000000453
Review Article: Carcinogenesis
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Survivin is one of the most cancer-specific proteins overexpressed in almost all malignancies, but is nearly undetectable in most normal tissues in adults. Functionally, as a member of the inhibitor of apoptosis family, survivin has been shown to inhibit apoptosis and increase proliferation. The antiapoptotic function of survivin seems to be related to its ability to inhibit caspases directly or indirectly. Furthermore, the role of survivin in cell cycle division control is related to its role in the chromosomal passenger complex. Consistent with its determining role in these processes, survivin plays a crucial role in cancer progression and cancer cell resistance to anticancer drugs and ionizing radiation. On the basis of these findings, recently survivin has been investigated intensively as an ideal tumor biomarker. Thus, multiple molecular approaches such as use of the RNA interfering technique, antisense oligonucleotides, ribozyme, and small molecule inhibitors have been used to downregulate survivin regulation and inhibit its biological function consequently. In this review, all these approaches are explained and other compounds that induced apoptosis in different cell lines through survivin inhibition are also reported.

aCellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord

bDepartment of Pathobiology, School of Veterinary Medicine, Division of Biotechnology, Shiraz University, Shiraz, Iran

Correspondence to Mohammad Chehelgerdi, Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran Tel: +98 910 177 1579; e-mail: chehelgerdi1992@gmail.com

Received February 26, 2018

Accepted March 18, 2018

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