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Objective: colorectal cancer (colorectal cancer, CRC) of common malignant tumors of the gastrointestinal tract, and showed a clear upward trend in the incidence and mortality. The incidence of colorectal cancer is a multi-factor, multi-step process, the formation of the corresponding phenotype of different pathological stage. Tumorigenesis and development is a series of molecular changes in normal cells by a variety of external factors, including biological, physical, chemical, and ultimately lead to changes in the phenotype, become a tumor. Tumorigenesis, is also the result of the imbalance of cell proliferation and apoptosis. The close relationship of the development of colorectal cancer and apoptosis. In the study of the mechanisms of apoptosis, it was found that the basic helix - loop - helix protein (basic helix-loop-helix bHLH) family of highly conserved Twist gene not only has the characteristics of the oncogene, but also through a variety of ways inhibit the process of apoptosis, promote the occurrence of epithelial - mesenchymal transition (EMT) and the formation of blood vessels, but also lead to the occurrence of tumor development. Studies have shown that in a variety of solid tumors (including breast cancer, prostate cancer, melanoma and osteosarcoma), Twist excessive expression can promote apoptosis in human breast cancer and melanoma cell lines. Study confirmed of Twist in human breast cancer MCF-7 cell line, colon cancer HCT116 cell lines 786-0 cell lines, gastric cancer the MNK cell strains, hepatoma HepG2 cells and normal liver cells LO2 six kinds of cell lines in highest expression in colon cancer HCT116 cell lines, and the lowest expression in normal liver cells LO2. Our previous study also showed that HCT116, SW480, SW620 three colon cancer cell lines, the highest expression of the Twist gene in HCT116 cell lines. In a previous study, we raised Twist gene expression, enhancement of human colon cancer SW480 cell lines in vitro proliferation and invasion and metastasis. In this study, the reduction in the expression of the Twist gene observed HCT116 cells in vitro proliferation and invasiveness of human colon cancer, to further determine the Twist gene and colorectal cancer, the development of the relationship. Methods: The study will be high expression of Twist siRNA interference plasmid and empty plasmid were transiently transfected into Twist colon cancer cell line HCT116 as interference and control groups, respectively, were screened by G418, identified through RT-PCR and Western-blot method observe Twist SiRNA success silent Twist gene expression in colon cancer HCT116 cells, and then measured by MTT assay and plotted interference and control groups cell growth curve, and then through the cell the scratches experimental and Transwell invasion assay, observation Twist gene on cell migration and invasion. Results: RT-PCR and Western blot results showed that: interference the group cells Twist gene expression levels significantly lower than the control group, the difference was statistically significant (P lt; 0.05) .2 by MTT cell growth curve, the results show, from the first four days, the cell growth rate of the interference group was significantly lower than the control group, the difference was statistically significant (P lt; 0.05). 3 the by cell scratch experiments show scratch after 24 hours, migration of control cells (25.24 ± 1.65)%, the interference group cell migration (15.06 ± 2.56)%, the difference was statistically significant. 48 hours later, the migration of control cells (45.37 ± 6.79)%, the interference group migration (25.77 ± 4.06)%, the difference was statistically significant (P lt; 0.05). 4 in vitro invasion assay results show that the number of control group cell invasion (123 ± 20), the number of cell invasion interference group (68 ± 18), the difference was statistically significant (P lt; 0.05). Conclusion: 1 using the experimental method can be successfully silencing in human colon cancer HCT116 cells Twist gene expression. 2 Twist silence gene expression, HCT116 cell proliferation rate decreased significantly, indicating the Twist gene can affect the in vitro proliferation of HCT116 cells. 3 Twist silence gene expression, HCT116 cells in vitro migration significantly decreased, indicating that the the Twist gene could affect HCT116 cell migration. The 4 silent Twist gene expression, HCT116 cells in vitro invasion capacity decreased significantly, indicating that the the Twist gene affect HCT1160 cells in vitro invasion ability.
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