AIM: To study the effect of SCUBE2 on epithelial-mesenchymal transition (EMT) in colorectal cancer cells and its mechanism .METHODS:The expression of SCUBE2 in human colorectal cancer cell line HCT 116 and normal colonic cell line FHC was detected by real-time PCR and Western blot .HCT116 cells were transfected with GV144-SCUBE2 to over-express SCUBE2, and then the cell viability, migration, and apoptosis were determined by MTT assay , Transwell assay and flow cytometry, respectively.The expression of EMT markers (E-cadherin, vimentin, and Snail),β-catenin, c-Myc and cyclin D1 in the HCT116 cells was analyzed by real-time PCR or Western blot after transfection with GV144-SCUBE2 for 6 h, followed by the stimulation of 10 μg/L recombinant TGF-β1 protein for 48 h.Additionally, the EMT process of HCT116 cells, which were stimulated by TGF-β1, over-expressed SCUBE2, and treated with Wnt/β-cate-nin pathway activator lithium chloride ( LiCl) or inhibitor XAV93920, was analyzed by Western blot .RESULTS: Com-pared with FHC cells , the expression of SCUBE 2 in the HCT116 cells was significantly decreased .The viability and migra-tion ability of the HCT116 cells were suppressed by SCUBE2 over-expression, but the apoptosis was not markedly changed . Elevated expression of SCUBE2 increased E-cadherin expression, and decreased the expression of vimentin, Snail,β-cate-nin, c-Myc and cyclin D1 induced by TGF-β1.Treatment with LiCl blocked but treatment with XAV 93920 enhanced the effects of SCUBE2 on EMT.CONCLUSION:Over-expression of SCUBE2 may inhibit the cell growth and migration , and suppress EMT through Wnt/β-catenin signaling pathway .

Ulcerative colitis （UC）， a chronic inflammatory bowel disease affecting the colorectum with high morbidity and prevalence， has become a global burden. However， the causes and pathogenesis are still unclear. Available studies have verified that the imbalance of intestinal microenvironment is crucial in the occurrence and development of UC. Intestinal microenvironment is mainly composed of intestinal microbiota and intestinal mucosal cells， which are involved in the physiological and pathological activities of the body through the intestinal microbial barrier， chemical barrier， mechanical barrier， and immune barrier. Thus， probiotic agents， 5-aminosalicylic acid preparations， corticosteroids， immunosuppressants， biological preparations and other drugs are commonly used in western medicine for the treatment of UC， which， however， have limitations. Therefore， it is the key task for the prevention and treatment of UC to find new therapies. In recent years， it has been found that traditional Chinese medicine （TCM） has unique advantages in the prevention and treatment of UC. Chinese medicine compounds and Chinese medicine monomers can regulate the intestinal microenvironment through multiple pathways and targets， thereby intervening the occurrence and development of UC. It has gradually become a hot spot in the prevention and treatment of UC and attracted extensive attention. Therefore， this study first discussed the correlation between intestinal microenvironment imbalance and UC and then summarized the mechanisms of TCM against UC from the aspects of regulating intestinal flora， improving chemical barrier， protecting mechanical barrier， and inhibiting immune inflammatory response， in order to provide new ideas for the research on TCM in the treatment of UC.

ObjectiveTo investigate the effect of curcumin on the cycle arrest of human colon cancer HCT116 cells and decipher the possible molecular mechanism. MethodThe methyl thiazolyl tetrazolium （MTT） method was employed to examine the effects of curcumin （0， 12.5， 25， 50， 75， 100 μmol·L^-1） and 5-fluorouracil （5-FU， 600 μmol·L^-1） on the proliferation of HCT116 cells at different time points （24， 48， 72 h）. Flow cytometry was employed to examine the cycle of HCT116 cells treated with curcumin （0， 25， 50， 75 μmol·L^-1） and 5-FU. Western blot was employed to determine the expression of proteins in the Janus kinase 1 （JAK1）/signal transducer and activator of transcription 1 （STAT1） /cyclin-dependent kinase inhibitor 1A （p21） pathway in HCT116 cells. The binding of STAT1 to p21 promoter region was detected by chromatin immunoprecipitation （ChIP）. Small interfering RNA （siRNA） was employed to measure the role of STAT1 in regulating the expression of p21 and that of JAK1 in regulating the activation of STAT1 by Western blot and cellular immunofluorescence， respectively. ResultCompared with the blank group， the HCT-116 cells treated with curcumin and 5-FU showed decreased viability （P<0.05）， increased proportions of cells in the G₀/G₁ phase （P<0.05）， decreased proportions of cells in the S phase and G₂/M phase （P<0.05）， down-regulated protein level of phosphorylated p21 （P<0.05）， and up-regulated protein level of p21 （P<0.05）. Compared with the curcumin group， the p21 siRNA+ curcumin group presented decreased proportion of cells in G₀/G₁ phase （P<0.05）. Compared with the blank group， curcumin elevated the level of phosphorylated STAT1 （p-STAT1） （P<0.05）. Compared with the curcumin group， the curcumin + STAT1 siRNA group showcased up-regulated protein level of p21 in HCT116 cells （P<0.05）. The mechanism study showed that curcumin treatment enhanced the enrichment of STAT1 in the p21 promoter region （P<0.05） compared with the blank group. Compared with the blank group， curcumin up-regulated the level of phosphorylated JAK1 （p-JAK1） （P <0.05）. Compared with the curcumin group， the curcumin + STAT1 siRNA group demonstrated up-regulated protein levels of p-STAT1 and p21 in HCT116 cells （P<0.05）. ConclusionCurcumin may induce the cycle arrest of human colon cancer HCT116 cells by activating the JAK1/STAT1/p21 signaling pathway.