ISPO

Estradiol induces G2/M cell cycle arrest and inhibits ATP synthase 6 levels in human stomach tumor cells (SC-M1)

WL Wang MSa, HC Ho PhDb, CC Su MDc, JG Chung PhDa

Department of Microbiology a and Biochemistryb,China Medical College, Taichung, Taiwan. Department of Surgery c, China Medical College Hospital, Taichung, Taiwan.

In this investigation, the effects of 17-apha-estradiol on viability, cell cycling, cyclins and ATP synthase 6 gene expression in human stomach adenocarcinoma cells (SC-M1) were examined. Viability, cell cycling, and cyclins were examined and determined by flow cytometric analysis to show the percentage of staining cells by propidium iodide and monoclonal antibody. The results indicate that 17-apha-estradiol induced cytotoxicity, G2/M cell cycle arrest and cyclin A expression in SC-M1 cells. The effects of cytotoxicity and cell cycle by 17-apha-estradiol were dose- and time-dependent. The concentration of 17-apha-estradiol affects cyclin A level was 60 microM. The ATP synthase 6 gene expression was examined by differential display RT-PCR. The results indicate that 17-apha-estradiol (60 microM) inhibit ATP synthase 6 gene expression in SC-M1 cells. In conclusion, 17-apha-estradiol did affect SC-M1 cells underwent the G2/M arrest and ATP synthase 6 (mitochondria) which led to cell death.

KEY WORDS: 17-apha-estradiol, G2/M cell cycle arrest, ATP synthase 6.

For more information, contact u966003@mail.cmc.edu.tw

Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Prevention.

http://www.cancerprev.org/Journal/Issues/26/101/1093/4560