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Influence of p53 and p21Waf1 expression on G2/M phase arrest of colorectal carcinoma HCT116 cells to proteasome inhibitors

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Affiliated Author(s)
박종욱권택규
Alternative Author(s)
Park, Jong WookKwon, Taeg Kyu
Journal Title
International Journal of Oncology
ISSN
1019-6439
Issued Date
2004
Abstract
Ubiquitin-mediated protein degradation in vertebrates has been implicated in cell cycle control. In this report we explored the effects of proteasome inhibitors (MG132, lactacystin and ALLN) on cell cycle distribution. Colorectal carcinoma HCT116 cells were treated with proteasome inhibitor MG132. The results showed that MG132 inhibited cell proliferation in a dose-dependent manner. MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21. MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53−/−) and HCT116 (p21−/−) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest. The release experiments from nocodazole-induced mitotic phase cells indicated that MG132 inhibits the proliferation of HCT116 cells via arrest in the G2 phase. In addition, when HCT116 cells were exposed to combination of sodium butyrate and MG132 enhanced cell growth inhibition and induction of apoptosis were observed.
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
On Hee Kim et al. (2004). Influence of p53 and p21Waf1 expression on G2/M phase arrest of colorectal carcinoma HCT116 cells to proteasome inhibitors. International Journal of Oncology, 24(4), 935–941. doi: 10.3892/ijo.24.4.935
Type
Article
ISSN
1019-6439
DOI
10.3892/ijo.24.4.935
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35929
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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