Roles of 14-3-3 eta in mitotic progression and its potential use as a therapeutic target for cancers
- Authors
- Lee, CG[Lee, C. G.]; Park, GY[Park, G-Y]; Han, YK[Han, Y. K.]; Lee, JH[Lee, J. H.]; Chun, SH[Chun, S. H.]; Park, HY[Park, H-Y]; Lim, KH[Lim, K-H]; Kim, EG[Kim, E-G]; Choi, YJ[Choi, Y-J]; Yang, K[Yang, K.]; Lee, CW[Lee, C-W]
- Issue Date
- 21-Mar-2013
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- 14-3-3; mitosis; cell death; aneuploid; caspase
- Citation
- ONCOGENE, v.32, no.12, pp.1560 - 1569
- Indexed
- SCIE
SCOPUS
- Journal Title
- ONCOGENE
- Volume
- 32
- Number
- 12
- Start Page
- 1560
- End Page
- 1569
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/61208
- DOI
- 10.1038/onc.2012.170
- ISSN
- 0950-9232
- Abstract
- 14-3-3 proteins are involved in several cellular processes, including the G1/S and G2/M cell cycle transitions. However, their roles during mitosis are not well understood. Here, we showed that depletion of 14-3-3 eta, a 14-3-3 protein isoform, enhanced mitotic cell death, resulting in sensitization to microtubule inhibitors and inhibition of aneuploidy formation. The enhanced mitotic cell death by depletion of 14-3-3 eta appeared to be both caspase-dependent and independent. Furthermore, enhanced mitotic cell death and a reduction in aneuploidy following 14-3-3 eta depletion were independent of the mitotic checkpoint, which is thought to be the primary signaling event in the regulation of the cell death induced by microtubule inhibitors. When 14-3-3 eta depletion was combined with microtubule inhibitors in HCT116 and U87MG cells, it sensitized both cancer cell lines to microtubule inhibitors. These results collectively suggest that 14-3-3 eta may be required for mitotic progression and may be considered as a novel anti-cancer strategy in combination with microtubule inhibitors. Oncogene (2013) 32, 1560-1569; doi:10.1038/onc.2012.170; published online 7 May 2012
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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