PT  - JOURNAL ARTICLE
AU  - HOSOKAWA, MAMI
AU  - KADOTA, RITSUKO
AU  - SHICHIJO, SHIGEKI
AU  - ITOH, KYOGO
AU  - DMITRIEV, IGOR
AU  - KRASNYKH, VICTOR
AU  - CURIEL, DAVID T.
AU  - TAKUE, YOICHI
AU  - WAKASUGI, HIRO
AU  - TAKASHIMA, SHIGEMITSU
AU  - HEIKE, YUJI
TI  - Cell Cycle Arrest and Apoptosis Induced by SART-1 Gene Transduction
DP  - 2005 May 01
TA  - Anticancer Research
PG  - 1983--1990
VI  - 25
IP  - 3B
4099  - http://ar.iiarjournals.org/content/25/3B/1983.short
4100  - http://ar.iiarjournals.org/content/25/3B/1983.full
SO  - Anticancer Res2005 May 01; 25
AB  - The biological function of the SART-1 gene product is demonstrated and its potential as a target for cancer gene therapy is discussed. Materials and Methods: The SART-1 gene was transduced by a recombinant adenovirus vector and its expression was promoted by a CMV promoter. Results: The transduction efficiency by recombinant adenoviruses in A549 and MCF-7 cells was determined using a vector expressing luciferase, which showed high expression in the cells. Cell count analysis using Trypan-Blue dye exclusion showed that SART-1 gene transduction inhibited cell growth. Flow cytometry analysis suggested that SART-1 gene transduction induced cell cycle arrest followed by apoptosis. Western blot analysis confirmed that the apoptosis pathway was activated by SART-1 gene transduction. Conclusion: These results show that SART-1 gene transduction induces cell cycle arrest leading to apoptosis and suggest the possibility of gene therapy against cancer. In addition, SART-1 is known to be a tumor antigen in a range of cancers recognized by T cells, thus a potential strategy would be the combination of suicide gene therapy with immuno-gene therapy. Copyright© 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved