PT  - JOURNAL ARTICLE
AU  - TANIGUCHI, KOICHI
AU  - MOMIYAMA, NOBUYOSHI
AU  - UEDA, MICHIO
AU  - MATSUYAMA, RYUSEI
AU  - MORI, RYUTARO
AU  - FUJII, YOSHIRO
AU  - ICHIKAWA, YASUSHI
AU  - ENDO, ITARU
AU  - TOGO, SHINJI
AU  - SHIMADA, HIROSHI
TI  - Targeting of CDC20 <em>via</em> Small Interfering RNA Causes Enhancement of the Cytotoxicity of Chemoradiation
DP  - 2008 May 01
TA  - Anticancer Research
PG  - 1559--1563
VI  - 28
IP  - 3A
4099  - http://ar.iiarjournals.org/content/28/3A/1559.short
4100  - http://ar.iiarjournals.org/content/28/3A/1559.full
SO  - Anticancer Res2008 May 01; 28
AB  - Background: Cell division cycle 20 homologue (CDC20), which encodes a protein that promotes chromosomal separation, is highly expressed in several carcinomas, including pancreatic cancer. Materials and Methods: To ascertain whether this gene could be a potential therapeutic target, the RNA interference technique was applied using small interfering RNA (siRNA) to knockdown CDC20 expression. Results: The CDC20 siRNA showed more than 90% inhibition of CDC20 expression at both the transcriptional and translational levels and the specific knockdown of CDC20 expression inhibited the cell growth of human pancreatic carcinoma cells in vitro. Suppression of CDC20 induced accumulation of the cells in the G2/M-phase of the cell cycle. In addition, the knockdown of CDC20 caused enhancement of the cytotoxicity of paclitaxel and increased the effect of γ-irradiation against pancreatic carcinoma cells. Conclusion: CDC20 is a promising target for gene specific therapy in human pancreatic cancer. Copyright© 2008 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved