Objective：To investigate the potential effects of long non-coding RNA（lncRNA）HOX transcript antisense intergenic RNA（HOTAIR）on proliferation，invasion and metastasis capacity of gastric cancer cells and to reveal the underling mechanisms. Methods：Human gastric epithelial cell line（GES-1）and different gastric cancer cell lines（SGC7901 and MKN-45）were cultured respectively. SGC7901 cancer cells were transiently transfected with small interfering RNA targeting HOTAIR（siHOTAIR），qRT-PCR was conducted to assess HOTAIR expression. MTT assay was carried out to evaluate the cell proliferation，wound-healing assay as well as transwell matrix invasion assay was performed respectively to evaluate the capability of invasion and migration of gastric cancer cells. The expression of cyclooxygenase-2（COX-2），together with E-cadherin was detected by Western blot assay. Results：The expression of HOTAIR in gastric cancer cells was higher than that in GES-1 cells（P < 0.05）. The cell proliferation was significantly inhibited after HOTAIR knockdown（P < 0.01）. Both wound healing assay and transwell assay demonstrated that HOTAIR knockdown resulted in a lower ratio in migration and invasion. Western blot analysis revealed that depletion of HOTAIR substantially decreased the expression of COX-2，and then elevated the expression of E-cadherin（P < 0.05），this effect would be attenuated by exogenous prostaglandin E2（PGE2）. Compared with siHOTAIR group，poliferation and invasion of SGC7901 cells were significantly increased in siHOTAIR + PGE2 group（P < 0.05）. Conclusion：Downregulation of lncRNA HOTAIR would inhibit cell viability，invasion and migration capability of gastric cancer cells，which were mediated partially by inhibiting the expression of COX-2 and then upregulating the expression of E-cadherin. HOTAIR might be a promising target to modulate the invasion and metastasis of gastric caner.