Background and purpose: ZNF139, a member of zinc finger protein family, is a transcription factor. Our previous studies have showed that the over-expression of ZNF139 in gastric cancer (GC) cells was related to the differentiation of GC. However, the function of ZNF139 in GC cells' apoptosis is still unclear. In present study, endogenous ZNF139 in GC cell line BGC823 was inhibited with siRNA, and then mechanism of ZNF139 in GC cells' apoptosis was investigated. Methods: Expression of ZNF139 in GC tissues, adjacent normal tissues, GC cell lines MKN28, SGC7901, BGC823 and that in gastric epithelial cell line GES-1 were tested. Then ZNF139-specific siRNA was transfected into BGC823 cells. Viability, cell cycle and apoptosis of GC cells were detected. Survivin, x-IAP, caspase-3, Fas, p53, Bcl-2 and Bax genes were detected with QPCR and Western blot. Results: ZNF139 expression in GC tissues was significantly higher than that in adjacent normal tissues; ZNF139 expression in GES-1 was very weak, but it expressed in various GC cell lines, with the highest expression in BGC823. After endogenous ZNF139 was inhibited with ZNF139-siRNA, FCM indicated that after transfection, GC cells in G0/G1 phase was significantly increased, but was significantly reduced in G2/M phases; also after transfection, the apoptotic rate of BGC823 cells increased significantly. 48 h after ZNF139-siRNA was transfected, the expression of Survivin, x-IAP and Bcl-2 was significantly down-regulated, while the expression of caspase-3 and Bax was significantly up-regulated. Conclusion: Our results suggest that ZNF139 functions to promote apoptosis resistance of BGC823 by regulating some apoptosis related genes.