Objective To investigate the role of long non-coding RNA (lncRNA)-ROR in mediating epithelial-mesenchymal transformation (EMT) and its impact on radiotherapy resistance in nasopharyngeal carcinoma cells. Methods Nasopharyngeal carcinoma cells CNE2 were divided into blank group, negative control (NC) group and lncRNA-ROR siliencing group; or were divided into blank group, radiotherapy group, radiotherapy＋NC group, and radiotherapy＋lncRNA-ROR overexpression group (radiotherapy treated with 6 Gy radiation for 24 h). The CNE2 proliferation was detected by cell counting kit 8 method. The cell migration was detected by cell scratch test and Transwell cell migration test. The apoptosis ratio was detected by flow cytometry, and the apoptosis-related proteins and epithelial-mesenchymal transition proteins were detected by Western blotting. Results Compared with the blank group and NC group, the proliferation ability of nasopharyngeal carcinoma cells CNE2 was decreased after inhibition of lncRNA-ROR expression for 48 and 72 h (all P＜0.05). The mobility of CNE2 cells after lncRNA-ROR expression inhibition was lower than that in the NC group (P＜0.05). The migration ability of CNE2 cells in the radiotherapy＋lncRNA-ROR overexpression group was higher than that in the radiotherapy group and radiotherapy＋NC group (both P＜0.05). Compared with the radiotherapy group and radiotherapy＋NC group, the apoptosis rates of CNE2 cells in the radiotherapy＋lncRNA-ROR overexpression group was decreased (both P＜0.05). After lncRNA-ROR inhibition, the expression of activated caspase 3 and caspase 9 proteins was increased (both P＜0.05), while the expression of activated caspase 3 and caspase 9 proteins was decreased in the radiotherapy＋overexpressed lncRNA-ROR group (both P＜0.05). Inhibition of lncRNA-ROR increased the expression of epithelial marker proteins (E-cadherin, β-catenin), and decreased the expression of interstitial marker proteins (N-cadherin, vimentin). The epithelial marker protein expression was decreased and interstitial marker protein expression was increased in CNE2 cells in the radiotherapy＋lncRNA-ROR overexpression group compared with the radiotherapy group and radiotherapy＋NC group (all P＜0.05). Conclusion lncRNA-ROR can affect the radiotherapy resistance of nasopharyngeal carcinoma cells by regulating their proliferation, migration, apoptosis and EMT, and it is a potential target for reversing the radiotherapy resistance of nasopharyngeal carcinoma cells.