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Objective: Lung cancer is the leading cause of cancer deaths worldwide due to poor overall prognosis,disease relapse and lacking of curative systemic therapy.MUC1 is overexpressed in more than 70% of human lung cancer with a loss of polarity,but the underline mechanisms of how MUC1 affects therapy of lung cancer remain to be explored.Herein,we try to elucidate the roles of MUC 1 in drug resistance of lung cancer.Methods: We established stable cell lines of lung cancer by silencing MUC 1 in NCI-H446 that expressing high level of MUC 1.CCK8 was applied to measure cell viability;co-IP and IF were employed to determine the interaction of proteins;flow cytometry was utilized to detect the cell cycle and appotosis after taxol treatment.Results: Our results show that silencing MUC1 is related to cell cycle delaying and increases sensitivity to Taxol.Silencing MUC1 leads to the G2/M arrest,continuous phosphorlation of BubR1 and the accumulation of Cyclin B1 when treated with taxol.Moreover,we find MUC1 can interact and co-localize with BubRl and PP2A,which can directly dephosphorylate BubR1.Conclusion: MUC1 renders lung cancer cell resistant to taxol by interacting with BubR1 and PP2A.