Background Bcl-2, the anti-apoptotic protein is overexpressed in the majority of gastric cancers and associated with its pathogenesis. To better understanding of the role of Bcl-2, RNA interference （RNAi） was used t...Background Bcl-2, the anti-apoptotic protein is overexpressed in the majority of gastric cancers and associated with its pathogenesis. To better understanding of the role of Bcl-2, RNA interference （RNAi） was used to inhibit Bcl-2 expression in the human gastric cancer cells in vitro and in vivo. Methods Bcl-2 small interfering RNA （siRNA） was transfected into human gastric cancer cells $GC-7901, and Bcl-2 expression was monitored by real-time polymerase chain reaction （PCR） and Western blot. Cell proliferation, apoptosis, and telomerase activity were examined by MTT, flow cytometry, and TRAP assay, respectively. Gastric cancer cells treated with 100 nmol/L Bcl-2 siRNA were subcutaneously transplanted into nude mice and tumor growth was assessed. Results Bcl-2 siRNA significantly inhibited the expression of Bcl-2 in human gastric cancer cells at both mRNA and protein levels in a time- and dose-dependent manner. Bcl-2 siRNA also decreased telomerase activity （by 78.76%） and increased the rate of apoptosis （by 37.47%）. SGC-7901 cell growth was also significantly suppressed in vivo and in vitro. Conclusions Bcl-2 expression knockdown suppressed the growth of gastric cancer cells. Thus, Bcl-2 may play a very important role in carcinogenesis of gastric cancer and its knockdown may offer a new potential gene therapy approach for human gastric cancer in future.展开更多
基金the grants from Shanghai Medical Key Discipline (No.05Ⅲ005)the National High Technology and Development Program of China(863 Program,No.2002BA7111A06).
文摘Background Bcl-2, the anti-apoptotic protein is overexpressed in the majority of gastric cancers and associated with its pathogenesis. To better understanding of the role of Bcl-2, RNA interference （RNAi） was used to inhibit Bcl-2 expression in the human gastric cancer cells in vitro and in vivo. Methods Bcl-2 small interfering RNA （siRNA） was transfected into human gastric cancer cells $GC-7901, and Bcl-2 expression was monitored by real-time polymerase chain reaction （PCR） and Western blot. Cell proliferation, apoptosis, and telomerase activity were examined by MTT, flow cytometry, and TRAP assay, respectively. Gastric cancer cells treated with 100 nmol/L Bcl-2 siRNA were subcutaneously transplanted into nude mice and tumor growth was assessed. Results Bcl-2 siRNA significantly inhibited the expression of Bcl-2 in human gastric cancer cells at both mRNA and protein levels in a time- and dose-dependent manner. Bcl-2 siRNA also decreased telomerase activity （by 78.76%） and increased the rate of apoptosis （by 37.47%）. SGC-7901 cell growth was also significantly suppressed in vivo and in vitro. Conclusions Bcl-2 expression knockdown suppressed the growth of gastric cancer cells. Thus, Bcl-2 may play a very important role in carcinogenesis of gastric cancer and its knockdown may offer a new potential gene therapy approach for human gastric cancer in future.
