cIAP2 (cellular inhibitor of apoptosis protein 2) is induced by NF-κB (nuclear factor κB) when cells need to respond quickly to different apoptotic stimuli. A recent study using cDNA microarray technology has suggested that cIAP2 transcription is regulated in a cell cycle-dependent manner, although the mechanism for such regulation is unknown. In this study, we confirmed the cell cycle-dependent regulation of cIAP2 expression at both the mRNA and protein levels. Additionally, we found that a bipartite CDE (cell cycle-dependent element)/CHR (cell cycle gene homology region) element in the cIAP2 promoter mediates cIAP2 gene activation in G2/M phase. Cell cycle-dependent G2/M-phase-specific cIAP2 expression is enhanced by NF-κB activation, and selective down-regulation of cIAP2 causes cells blocked in mitosis with nocodazole to become susceptible to apoptosis, indicating that the G2/M-phase-specific expression of cIAP2 contributes to the survival of mitotically arrested cells. Our studies describing the NF-κB-independent G2/M-phase-specific expression of cIAP2 will help in further understanding the molecular basis of cIAP2 over-expression in a variety of human cancers.
Research Article| September 27 2006
Cell cycle-dependent expression of cIAP2 at G2/M phase contributes to survival during mitotic cell cycle arrest
Tae H. Lee
Tae H. Lee 1
1Department of Biology, Yonsei University, Seoul 120-749, Korea, and Protein Network Research Center, Yonsei University, Seoul 120-749, Korea
1To whom correspondence should be addressed (email email@example.com).
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Hyung-Seung Jin, Tae H. Lee; Cell cycle-dependent expression of cIAP2 at G2/M phase contributes to survival during mitotic cell cycle arrest. Biochem J 15 October 2006; 399 (2): 335–342. doi: https://doi.org/10.1042/BJ20060612
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