A novel cervical cancer suppressor 3 (CCS-3) interacts with the BTB domain of PLZF and inhibits the cell growth by inducing apoptosis
- Authors
- Rho, SB[Rho, Seung Bae]; Park, YG[Park, Young Gyo]; Park, K[Park, Kyoungsook]; Lee, SH[Lee, Seung-Hoon]; Lee, JH[Lee, Je-Ho]
- Issue Date
- 24-Jul-2006
- Publisher
- ELSEVIER SCIENCE BV
- Citation
- FEBS LETTERS, v.580, no.17, pp.4073 - 4080
- Indexed
- SCIE
SCOPUS
- Journal Title
- FEBS LETTERS
- Volume
- 580
- Number
- 17
- Start Page
- 4073
- End Page
- 4080
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/87003
- DOI
- 10.1016/j.febslet.2006.06.047
- ISSN
- 0014-5793
- Abstract
- Promyelocytic leukemia zinc finger protein (PLZF) is a sequence-specific, DNA binding, transcriptional repressor differentially expressed during embryogenesis and in adult tissues. PLZF is known to be a negative regulator of cell cycle progression. We used PLZF as bait in a yeast two-hybrid screen with a cDNA library from the human ovary tissue. A novel cervical cancer suppressor 3 (CCS-3) was identified as a PLZF interacting partner. Further characterization revealed the BTB domain as an interacting domain of PLZF. Interaction of CCS-3 with PLZF in mammalian cells was also confirmed by co-immunoprecipitation and in vitro binding assays. It was found that, although CCS-3 shares similar homology with eEF1A, the study determined CCS-3 to be an isoform. CCS-3 was observed to be down-regulated in human cervical cell lines as well as in cervical tumors when compared to those from normal tissues. Overexpression of CCS-3 in human cervical cell lines inhibits cell growth by inducing apoptosis and suppressing human cyclin A2 promoter activity. These combined results suggest that the potential tumor suppressor activity of CCS-3 may be mediated by its interaction with PLZF. (c) 2006 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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