RT Journal Article SR Electronic T1 Cell Cycle Arrest and Apoptosis Induced by SART-1 Gene Transduction JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 1983 OP 1990 VO 25 IS 3B A1 HOSOKAWA, MAMI A1 KADOTA, RITSUKO A1 SHICHIJO, SHIGEKI A1 ITOH, KYOGO A1 DMITRIEV, IGOR A1 KRASNYKH, VICTOR A1 CURIEL, DAVID T. A1 TAKUE, YOICHI A1 WAKASUGI, HIRO A1 TAKASHIMA, SHIGEMITSU A1 HEIKE, YUJI YR 2005 UL http://ar.iiarjournals.org/content/25/3B/1983.abstract 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