Objective: To investigate the reversal effect of epigallocatechin gallate (EGCG) on radiotherapy-resistant cells of human nasopharyngeal carcinoma and the related mechanisms.Methods: Through in vitro experiments, the cell morphology and radiosensitivity of C666-1 and C666-1R were compared to verify the radioresistance of C666-1R. Further intervention with EGCG was adopted. Through CCK-8, flow cytometry and qPCR/Western blot detection, the mechanism by which EGCG reverses radiotherapy resistance by regulating proliferation and apoptosis-related factors was explored. Results:Morphological and functional experiments confirmed that C666-1R cells have significant radiation resistance: they have strong morphological heterogeneity, and there is no significant change in the proliferation rate after radiotherapy. Further research has found that EGCG inhibits the proliferation of C666-1R cells in a dose-dependent manner, with 150 μg/mL being the optimal intervention concentration. Mechanism studies have shown that EGCG combined with radiotherapy can significantly inhibit cell proliferation and reduce the expressions of Cyclin D1 and Ki-67. Meanwhile, it promotes cell apoptosis by up-regulating Bax and down-regulating Bcl-2, indicating that EGCG can effectively reverse the radiotherapy resistance of C666-1R cells.Conclusion: EGCG significantly reverses radioresistance in C666-1R nasopharyngeal cancer cells by inhibiting cell proliferation, and promoting apoptosis. The mechanism involves downregulating proliferation-related proteins Cyclin D1 and Ki-67, increasing the pro-apoptotic protein Bax, and decreasing the anti-apoptotic protein Bcl-2. EGCG provides a new potential therapeutic strategy to overcome radioresistance and improve therapeutic efficacy in NPC.