BMB Reports 2017; 50(7): 361-366  https://doi.org/10.5483/BMBRep.2017.50.7.185
Survivin protects fused cancer cells from cell death
Mihyang Do1,2,3, In-Hae Kwak1, Ju-Hyun Ahn1,2,3, In Jeong Lee1 & Jae-Ho Lee1,2,3,*
1Department of Biochemistry and Molecular Biology, 2Genomic Instability Research Center, Ajou University School of Medicine, 3Department of Biomedical Sciences, The Graduate School, Ajou University, Suwon 16499, Korea
Correspondence to: Tel: +82-31-219-5053; Fax: +82-31-219-5059; E-mail: jhlee64@ajou.ac.kr
Received: October 28, 2016; Revised: November 17, 2016; Accepted: February 14, 2017; Published online: July 31, 2017.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
Tetraploidy, a potential precursor of cancer-associated aneuploidy, is produced either by cell fusion or failure of cytokinesis. In this study, low p53-expressing HeLa cells were used to address the fate of cancer cells after fusion. We found that massive cell death or growth arrest occurred a few days after fusion. Interestingly, cells with larger nuclei preferentially died after fusion, suggesting that a larger deviation of DNA content is a strong inducer of apoptosis. Notably, a fraction of cells escaped cell death. Also, the stability of survivin increased, and its localization changed preferentially to the cytosol in fused cells. Knockdown of survivin decreased the survival of fused cells, more than observed in unfused cells, showing increased dependency of fused cells on survivin. Collectively, after cancer cell fusion, some fused cells avoid the apoptotic crisis partly owing to survivin, and continue to proliferate, a process that contributes to human cancer progression.
Keywords: Apoptosis, Cell death, Cell fusion, Proliferation, Survivin


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