Objective To investigate the role of TRIP13 in NSCLC and its related mechanisms. Methods The difference of trip13 expression between NSCLC and paracancerous lung was compared by immunohistochemistry, and the relationship between trip13 expression and clinicopathological features was analyzed. Human lung cancer cell line H1299 was divided into experimental group si-TRIP13-1, si-TRIP132 and negative control group(si-NC) by using siRNA transfection, and untreated H1299 cells were set as normal control group. The transfection effect of siRNA was detected by RTPCR and Western blot. MTT and Transwell experiments were used to determine the cell proliferation and invasion ability between experimental group and negative control group. Finally, Western blot was used to detect the expression of betacatenin, a key molecule of Wnt/βcatenin signaling pathway, and its downstream target proteins cyclin D1 and survivin in experimental and negative control cells.=Results=The expression of TRIP13 in NSCLC was significantly higher than that in normal lung tissue (P＜0.05). In NSCLC, the positive expression rate of TRIP13 was only significantly correlated with the degree of tumor differentiation, lymph node metastasis and TNM stage (P＜0.05). After transfection of siTRIP13 into lung cancer cell line H1299, the gene expression of si-TRIP13-1 and siTRIP132 in the experimental group was significantly lower than that in the negative control group and the normal control group (P＜0.05). Compared with the negative control group, the proliferation (P＜0.01), invasiveness (P＜0.05) of the cells in the siTRIP13 experimental group were significantly inhibited, and the expression of betacatenin, cyclin D1, survivin in the Wnt/βcateninsignaling pathway was significantly inhibited. The expression level of survivin protein also decreased significantly (P＜0.05). Conclusion TRIP13 may enhance the proliferation and invasion of NSCLC cells through Wnt/βcatenin signaling pathway to promote the occurrence and development of NSCLC.