Abstract: OBJECTIVE To investigate the effect of (-)-epigallocatechin-3-gallate(EGCG) on lung adenocarcinoma cell growth and to explore the mechanism of Ku70 in promoting apoptosis of lung cancer cells by EGCG. METHODS Construction of pSliencer 4.1-CMV-shKu70 plasmid interfered with the expression of Ku70 and established cell lines. Induction of apoptosis was examined by MTT method and Annexin V/PI double staining flow cytometry. Western blot analysis was used to detect the protein expression of cleaved Bax, caspase-3(17 kDa) and Ku70. Immunoprecipitation was used to detect the interaction between Ku70 and Bax. RESULTS EGCG significantly inhibited the the proliferation of A549(P<0.01), and EGCG could induce apoptosis of A549 cells(P<0.05), up-regulate the expression of Bax and caspase-3 and down-regulate the expression of Ku70. After the expression of Ku70 was inhibited, the effect of EGCG on the proliferation inhibition and apoptosis promotion of A549 cells was more obvious, and the expression of caspase-3 was further up-regulated, the levels of proteins changes were significantly(P<0.05), but the Bax level was not significantly changed. At the same time, EGCG could interfere the interaction between Ku70-Bax(P<0.05). CONCLUSION EGCG may inhibit proliferation and induce apoptosis in lung adenocarcinoma cell. The mechanism is related to inhibition of Ku70 expression, inhibition of interaction between Ku70-Bax, activation of Bax, and initiation of caspase cascade.