Published online Dec 15, 2000. doi: 10.3748/wjg.v6.i6.855
Revised: April 19, 2000
Accepted: April 26, 2000
Published online: December 15, 2000
AIM: To evaluate the potential of RA-538 gene therapy for gastric carcinoma.
METHODS: Human gastric carcinoma cell line SGC7901 treated with Ad-RA538 or Ad-LacZ were analysed by X-gal stain, MTT, DNA ladder, Tunel, flow cytometric analysis, PCR, and Western Blot in vitro. The tumorigenicity and experimental therapy in nude mice model were assessed in vivo.
RESULTS: Ad-LacZ could efficiently transfer the LacZ gene into SGC7901 cells. X-gal-positive cells at MOI 25, 50, 100, and 200 were 90%, 100%, 100%, and 100% respectively. Ad RA538 could strongly inhibit cell growth and induced apoptosis in SGC7901 cells. The proliferation of the Ad-RA538-in fected SGC7901 cells was reduced by 76.3%. The mechanism of killing of gastric carcinoma cells by Ad-RA538 was found to be apoptosis by DNA ladder, Tunel and flow cytometric analysis. The tumorigenicity in nude mice using Ad-RA538 showed that all three mice failed to form tumor from 7 to 30 d compared with Ad-LacZ and parent SGC7901 cells. Experimental therapy on the nude mice model bearing subcutaneous tumor of SGC7901 cells showed that intratumor instillation of Ad-RA538 inhibited the growth of the tumors. Ad-RA538-treated tumors were inhibited by 60.66%, compared with that of the tumor injected with Ad-LacZ and mock.
CONCLUSION: The expression of Ad-RA538 can inhibit growth and induce apoptosis of gastric cancer cell in vitro and in vivo. Ad-RA538 can be used potentially in gene therapy for gastric carcinoma.