Axin1 Expression Facilitates Cell Death Induced by Aurora Kinase Inhibition Through PARP Activation
- Authors
- Choi, Eun-Jin; Kim, Shi-Mun; Song, Ki-Joon; Lee, Jae-Myun; Kee, Sun-Ho
- Issue Date
- 9월-2011
- Publisher
- WILEY-BLACKWELL
- Keywords
- AXIN; AURORA KINASE; CELL DEATH; PARP; AIF
- Citation
- JOURNAL OF CELLULAR BIOCHEMISTRY, v.112, no.9, pp.2392 - 2402
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF CELLULAR BIOCHEMISTRY
- Volume
- 112
- Number
- 9
- Start Page
- 2392
- End Page
- 2402
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/111643
- DOI
- 10.1002/jcb.23162
- ISSN
- 0730-2312
- Abstract
- Axin, a negative regulator of Wnt signaling, participates in apoptosis, and Axin1 localizes to centrosomes and mitotic spindles, which requires Aurora kinase activity. In this study, Aurora inhibition of Axin1-expressing cells (L-Axin) produced polyploid cells, which died within 48 h posttreatment, whereas Axin2-expressing cells (L-Axin2) survived the same period. These cell death events showed apoptotic signs, such as chromatin condensation and increased sub-G1 populations, as well as cell membrane rupture. Further analysis showed that Aurora kinase inhibitor (AKI) treatment of L-Axin cells induced poly(ADP-ribose) polymerase (PARP) activation, which increased the poly(ADP-ribosyl) ation of cellular proteins and reduced cellular ATP content. PARP inhibition reduced a proportion of dead cells, suggesting PARP involvement in AKI-induced cell death. Also, AKI treatment of L-Axin cells induced mitochondrial apoptosis-inducing factor (AIF) release, but not mitochondrial cytochrome c release or caspase-3 activation. Knockdown of AIF attenuated AKI-induced cell death in L-Axin cells. Thus, our results suggest that Axin1 expression renders L929 cells sensitive to Aurora inhibition-induced cell death in a PARP-and AIF-dependent manner. J. Cell. Biochem. 112: 2392-2402, 2011. (C) 2011 Wiley-Liss, Inc.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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