Objective To investigate the mechanism of long⁃chain non⁃coding RNA（LncRNA）HOX transcript antisense RNA（HOTAIR）targeting microRNA ⁃30d（miR ⁃30d）on invasion and migration of nasopharyngeal carcinoma cells. Methods HOTAIR siRNA was transfected into CNE ⁃2 cells of nasopharyngeal carcinoma. Real ⁃ time quantitative polymerase chain reaction（RT⁃qPCR）was performed to measure the transfection effect. Transwell assay was carried out to measure the invasion and migration abilities of tumor cell.Western blot was used to detect the expression of epithelial cadherin，vimentin and glucose regulatory protein78（GRP78）in the cells. Bioinformatics software was used to analyze the binding sites of HOTAIR and miR⁃30d. The binding relationship was determined by double luciferase reporting system.RT⁃qPCR was used to detect the change of miR⁃30d expression after HOTAIR was down⁃regulated in nasopharyngeal carcinoma cells. HOTAIR siRNA and miR⁃30d inhibitor were co⁃transfected into CNE⁃2 cells.The changes of cell invasion and migration were analyzed by the above methods，as well as the expression of E⁃cadherin，vimentin and GRP78 proteins. Results After knocking down the expression of HOTAIR，the invasion and migration abilities of CNE⁃2 cells were decreased；the levels of vimentin and GRP78 were decreased but the level of E⁃cadherin was increased.HOTAIR regulated specifically the expression of miR⁃30d. The knock⁃down of HOTAIR expression could increase the level of miR⁃30d in CNE⁃2 cells.The miR⁃30d inhibitor significantly reversed the effects of HOTAIRsiRNA on invasion and migration abilities of CNE⁃2 cells and the expression of E⁃cadherin，vimentin and GRP78 proteins. Conclusion HOTAIR affects the expression of GRP78 and EMT⁃related proteins by negatively regulating miR⁃30d，