Background Bcl-2,the anti-apoptotic protein is overexpressed in the majority of gastric cancers and associated with itspathogenesis.To better understanding of the role of Bcl-2,RNA interference(RNAi)was used to inhibit Bcl-2 expressionin the human gastric cancer cells in vitro and in vivo.Methods Bcl-2 small interfering RNA(siRNA)was transfected into human gastric cancer cells SGC-7901,and Bcl-2expression 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 cellstreated 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 andprotein levels in a time-and dose-dependent manner.Bcl-2 siRNA also decreased telomerase activity(by 78.76%)andincreased 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 veryimportant role in carcinogenesis of gastric cancer and its knockdown may offer a new potential gene therapy approach forhuman gastric cancer in future. Background Bcl-2, the anti-apoptotic protein is overexpressed in the majority of gastric cancers and associated with its pathogenesis. 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 SGC-7901, and Bcl-2 expression was monitored by real-time polymerase chain reaction proliferation, apoptosis, and telomerase activity were examined by MTT, flow cytometry, and TRAP assay, respectively. Gastric cancer cellstated with 100 nmol / L Bcl-2 siRNA were subcutaneously transplanted into nude mice and tumor growth was found. 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 rates 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 role in carcinogenesis of gastric cancer and its knockdown may offer a new potential gene therapy approach forhuman gastric cancer in future.