Objective：The current study aims to explore the biological function of CCT2(chaperonin containning TCP1，subunit 2) in human lung adenocarcinoma. Methods：The expression divergence of CCT2 in lung adenocarcinoma tissues and normal lung tissue samples were analyzed from TCGA and GTEx database. The relationship between the expression level of CCT2 and the patient’s prognosis was evaluated through survival analysis. The expression of CCT2 in lung adenocarcinoma cells was measured by Reverse Transcription-Polymerase Chain Reaction(qRT-PCR)and Western blot. CCT2 siRNA was transfected into cell strains(A549，H1650 or H1299)respectively，which were divided into Group si - NC(negative control group)and Group si - CCT2(transfection group). Transfection efficiency was detected by qRT-PCR and Western blot. The proliferation ability of lung adenocarcinoma cell was tested by CCK-8. The cellular migration ability was detected by wound-healing experiment. The expression levels of CCT2 and Ki-67 in 72 cases of lung adenocarcinoma tissues were detected with immunohistochemical method，and the correlation between their expression levels and clinical pathology features were analyzed. Results：The results showed that，compared with normal lung tissues，the expression level of CCT2 in lung adenocarcinoma tissue was higher，which was related to low overall survival rate of lung adenocarcinoma patients (P＜0.05). According to qPCR and Western blot test，CCT2 highly expressed in lung adenocarcinoma cell，and the immunohistochemistry result showed that the CCT2 expression was positively correlated with the Ki-67 expression(P＜0.05). CCK-8 test results showed that the proliferation ability of A549 and H1650 cells in si-CCT2 group was significantly lower than that in the si- NC group 48 hours after siRNA transfection(P ＜ 0.05). The results of cell scratch test showed that the migration rate of A549 and H1650 cells in the si-CCT2 group was lower than that in the si-NC group 24 hours after siRNA transfection(P ＜ 0.05). Conclusion： The expression levels of CCT2 in lung adenocarcinoma cells and tissues increases. Knocking down its expression can inhibit the proliferation and migration of A549 and H1650 lung adenocarcinoma cells.