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A novel cervical cancer suppressor 3 (CCS‐3) interacts with the BTB domain of PLZF and inhibits the cell growth by inducing apoptosis
Author(s) -
Rho Seung Bae,
Park Young Gyo,
Park Kyoungsook,
Lee Seung-Hoon,
Lee Je-Ho
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.06.047
Subject(s) - biology , cell growth , cancer research , microbiology and biotechnology , immunoprecipitation , suppressor , cell culture , cell cycle , repressor , apoptosis , transcription factor , cancer , genetics , gene
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 downregulated 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.