Objective: To investigate the expression of the long non-coding RNA (lncRNA) CCAT2 in gastric cancer cells and its actions. Methods: The expressions of CCAT2 in different gastric cancer cell lines (AGS, Hs746T and BSG823) and normal gastric mucosal GES-1 cells were detected by qRT-PCR. The gastric cancer AGS cells were transfected with CCAT2 siRNA (si-CCAT2 group) or scrambled siRNA sequences (negative control group) respectively, and then their proliferative abilities were measured by CCK-8 assay, using untransfected AGS cells as blank control. In si-CCAT2 group and negative control group, the apoptosis, the migration and invasion abilities and the expressions of apoptosis-associated proteins were determined by flow cytometry, scratch assay, Transwell assay and Western blot analysis, respectively. Results: The relative expression levels of CCAT2 in all studied gastric cancer cell lines were significantly higher than that in the normal gastric mucosal GES-1 cells (all P<0.05). At 72 and 96 h after transfection, the proliferative ability in si-CCAT2 group was significantly lower than that in negative control group or blank control group (all P<0.05), while, no significant difference in proliferative ability was noted between negative control group and blank control group at each predefined time point (all P>0.05). In si-CCAT2 group compared with negative control group, the apoptosis rate was increased, and the wound healing rate and the number of invading cells were decreased significantly (all P<0.05); the protein expressions of P53, caspase-8 and Bax were up-regulated, while the protein expression of Bcl-2 was down-regulated significantly (all P<0.05). Conclusion: CCAT2 expression is increased in gastric cancer cells. Knockdown of its expression can inhibit the proliferation and abilities of migration and invasion of the gastric cancer cells, and the mechanism may be related to its regulating the expressions of apoptosis-associated proteins.