Cell cycle arrest and apoptosis induced by SART-1 gene transduction

Mami Hosokawa, Ritsuko Kadota, Shigeki Shichijo, Kyogo Itoh, Igor Dmitriev, Victor Krasnykh, David T. Curiel, Yoichi Takue, Hiro Wakasugi, Shigemitsu Takashima, Yuji Heike

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1983-1990
Number of pages8
JournalAnticancer research
Volume25
Issue number3 B
StatePublished - May 2005

Keywords

  • Apoptosis
  • Cell cycle
  • SART-1
  • Tumor rejection antigen

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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