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Autophagy has been recently suspected to plays an important role in the regulation of cancer development and the response of tumor cells to anticancer therapy.However, recent studies showed that autophagy have diametrically opposite consequences in cancer.Rubicon is an important autophagy inhibitor which binds to Beclinl during the maturation of autophagosome.Moreover, the role of Rubicon in the regulation of cancer development is still not clear.To make it clear the role of Rubicon in cancer, we investigated the expression of Rubicon in lung cancer and the effect of Rubicon overexpression on cell proliferation and tumor formation in a lung cancer cell lines.A total of 80 lung cancer cases, including squamous cell carcinoma cases (n=32), adenocarcinoma cases (n=32), bronchioloalveolar carcinoma (n=4), large cell carcinoma (n=4) and small cell undifferentiated carcinoma (n=8) were selected and subjected to immunohistochemical analysis for Rubicon protein expression.10 normal lung tissues were used as negative control.Rubicon expression level is much lower in lung cancer tissues than normal, especially in bronchioloalveolar carcinoma and small cell undifferentiated carcinoma.Furthermore, we observed that overexpression of Rubicon inhibits lung cancer cell proliferation and migration.Forced expression of Rubicon induces cancer cells apoptosis and necrosis.Rubicon overexpression sensitizes cancer cells to chemotherapy both in autophagy dependent and independent manner.These results suggest that Rubicon is a tumor repressor and a potential therapeutic target for lung cancer.Our studies first reveal the important role of Rubicon in lung cancer development and and this might provide new therapeutic approach for lung cancer.