Objective To investigate the effects of Twist on epithelial-mesenchymal transition (EMT), tumor stem cell phenotype transformation, and chemotherapy resistance in colorectal cancer HCT116 cells. Methods Human colon cancer HCTl 16 cells were selected and divided into the empty vector group and Twist overexpression group (Twist group). HCT116 cells in the empty vector group and Twist group were transfected with 2 μg of empty vector pcDNA3. 1 or pcDNA3. 1-Twist vector. The morphological observation and transwell assay were used to detect the invasive ability of cells. Western blotting and immunofluorescence were used to detect EMT markers E-cadherin and vimentin expression. Western blotting was used to detect the expression of tumor stem cell markers Bmil, Nanog and CD44. The HCT116 cells were given a chemotherapy drug oxaliplatin (0-10 μ,mol/L gradient concentration) and the cell viability was measured at 570 nm. P-gp protein expression was detected by Western blotting. The expression levels of ABCBl, ABCCl, ABCC2, ABCC3, ABCC4, ABCC5, ABCG2, ERCCl, XRCCl, MSH2, TUBB3, POLH, GSTπ and γ-GT1 were detected by real-time PCR. Results The morphology of HCT116 cells in the Twist group was differentiated from round to long spindle. The number of invasive cells in the empty vector group and Twist group were (6. 24 ± 0. 89) and (26. 83 ± 1. 02)/HP, respectively (P < 0. 05). The relative expression levels of EMT-related molecular protein E-cadherin in the empty vector group and Twist group were 0. 82 ± 0. 09 and 0. 24 ± 0. 04, respectively. The relative expression levels of vimentin were 0. 12 ± 0. 02 and 1. 05 ±0.12, respectively, with statistically significant difference in the protein expression (P <0. 05). The number of nucleation of HCT116 cells in the empty vector group and Twist group were (2. 43 ± 0. 14) and (10. 19 ± 0. 58) / HP, respectively (P <0. 05). The relative expression of Nanog in the empty vector group and the Twist group were 0. 06 ± 0. 01 and 0. 88 ± 0. 07, respectively. The relative expression levels of Bmil were 0. 23 ± 0. 04 and 1. 26 ± 0. 88, respectively. The relative expression of CD44 was 1. 45 ± 0. 09 and 8. 92 ± 0. 89, respectively; with statistically significant difference in the expression of Nanog, Bmil and CD44 between these two groups, all P < 0. 05. In the Twist group, the cell viability was 1.00±0.08, 0.84±0.09, 0.70±0.10, 0.53±0.07, 0.48±0.06 after stimulating at O, 0.1, 1, 5, and 10 μ,mol/L, respectively, and 1. 00 ± 0. 07, 0. 76 ± 0. 08, 0. 58 ± 0. 05, 0. 27 ± 0. 04, and 0. 08 ± 0. 04, in the vector group, respectively; statistically significant difference was found in the viability of oxaliplatin at different concentrations of HCT116 cells, all P < 0. 05. After oxaliplatin stimulation, the relative expression levels of ABCBl, ABC Cl, ABCC2, ABCC3, ABCC4, ABCC5, ABCG2, ERCCl, XRCCl, MSH2, TUBB3, POLH, GSTπ, γ-GTl increased in the Twist group. The expression levels of them in the Twsit group were 3. 20 ± 0. 35, 1. 10 ± 0. 11, 1. 14 ± 0. 18, 1. 09 ± 0. 09, 0. 88 ± 0. 09, 1. 09 ± 0. 12, 1. 30 ± 0. 14, 0. 98 ± 0. 10, 1. 02 ± 0. 13, 1. 13 ± 0. 08, 1. 42 ± 0. 25, 1. 09 ± 0. 08 0. 92 ± 0. 10, 1. 29 ± 0. 35, respectively, and they were 1 ± 0. 10, 1 ± 0. 14, 1 ± 0. 13, 1 ± 0. 15, 1 ± 0. 09, 1 ± 0. 12, 1 ± 0. 11, 1 ± 0. 15, 1 ± 0. 14, 1 ± 0. 13, 1 ± 0. 15, 1 ± 0. 09, 1±0. 15, and 1 ± 0. 17, respectively, in the empty vector group, with statistically significant difference in the ABCBl expression between the two groups (all P < 0. 05). Conclusion Twist can promote EMT and stem cell phenotype switching in colorectal cancer HCT116 cells and up-regulate the chemosensitivity of HCT116 cells . [ABSTRACT FROM AUTHOR]