Objective To investigate the effect of hnRNPAB overexpression on epithelial-mesenchymal transformation(EMT) and its molecular mechanism using human colorectal cancer line SW480 and HT29. Methods SW480 and HT29 cells were infected with lentivirus overexpressing hnRNPAB and negative control virus to generate the corresponding cell lines in experimental group (SW480-hnRNPAB, HT29-hnRNPAB) and control group (SW480-NC, HT29-NC). To quantify the levels of hnRNPAB and EMT-related indicators (E-cadherin, N-cadherin and vimentin), RT-qPCR and Western blotting were used. Cell migration was measured using the scratch assay. Cell invasion was evaluated using the Transwell assay. Western blotting was used to detect the expression levels of Wnt/β-catenin signaling key indicators WNT3A, WNT5A and β-catenin. Results Compared with control group, the expression levels of hnRNPAB mRNA and protein in experimental group significantly increased, and the differences were statistically significant (P<0.01). The scratch healing rates in experimental group were significantly higher than that in control group (SW480: 19.6%±0.90% vs. 2.23%±0.80%, P<0.01; HT29: 40.30%±0.70% vs. 6.40%±0.06%, P<0.01). The number of Transwell cells was significantly higher than that in control group [SW480: (315.0±6.7) cells vs. (62.0±4.3) cells, P<0.01; HT29:(289.0±7.2) cells vs. (54.0±5.2) cells, P<0.01]. Compared with control group, the epithelial cell marker E-cadherin mRNA and protein expression levels in experimental group significantly decreased. As expected, the mesenchymal cell markers N-cadherin and vimentin mRNA and protein levels significantly increased, and the differences were statistically significant (P<0.01). Compared with control group, the expressions of WNT3A, WNT5A and β-catenin protein in experimental group significantly increased (P<0.01). Conclusions The overexpression of hnRNPAB could induce EMT of human colorectal cancer SW480 and HT29, demonstrated by enhanced cell migration and invasion ability. The mechanism may be related to the activation of the Wnt/β-catenin signaling pathway.