RT Journal Article SR Electronic T1 Targeting of CDC20 via Small Interfering RNA Causes Enhancement of the Cytotoxicity of Chemoradiation JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 1559 OP 1563 VO 28 IS 3A A1 TANIGUCHI, KOICHI A1 MOMIYAMA, NOBUYOSHI A1 UEDA, MICHIO A1 MATSUYAMA, RYUSEI A1 MORI, RYUTARO A1 FUJII, YOSHIRO A1 ICHIKAWA, YASUSHI A1 ENDO, ITARU A1 TOGO, SHINJI A1 SHIMADA, HIROSHI YR 2008 UL http://ar.iiarjournals.org/content/28/3A/1559.abstract 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