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0.05),but the MLD values at the tumor margin were significantly higher than that of normal mucosa(P
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Objective To investigate the effect of caffeic acid phenethyl ester (CAPE) on the growth of human colorectal carcinoma cell line HCT116 transplanted subcutaneously in nude mice. Methods Nude mouse model of human colorectal carcinoma by subcutaneous transplantation of HCT116 cell line was reproduced. A total of 20 mice were divided into 2 groups: control group and CAPE group (oral administration of CAPE at 5mg/mice/d). The growth of the subcutaneously transplanted tumor and changes in mouse body weight in each group after treatment were observed on 7, 14, 21 and 28d. Histopathological examination of xenograft, heart, liver, lung, kidney and intestine of nude mice was also conducted. Apoptosis index was detected by terminal dUTP nick end labeling (TUNEL) technique. Results CAPE had significantly inhibitory effect on growth of the transplanted xenograft in vivo. Tumor volume and tumor weight were decreased (P
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Objective To study the effect of caffeic acid phenethyl ester (CAPE) on the expression of ?-catenin in the cultured colorectal cancer cell lines. Methods HCT116 and W480 cells were treated with CAPE at serial concentrations of 2.5, 5, and 10 mg/L. ?-catenin protein expression was assayed by Western blot analysis. ?-catenin localization was detected by indirect immunofluorescence. Results CAPE treatment was associated with decreased total ?-catenin protein expression. The expression of ?-catenin at the cell nucleus and cytoplasm was downregulated, but at the cell-cell linked site the ?-catenin protein expression was upregulated. Conclusion CAPE can downregulate the expression of ?-catenin and inhibit the translocation of ?-catenin to nucleus, which may play an important role in the anticancer activity of CAPE.
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Objective To investigate the role of APE1 in the carcinogenesis and progression of colorectal carcinoma (CRC). Methods Expression of APE1 was determined with SP immunohistochemical technique in 40 specimens of normal colorectal mucosa, 60 specimens of colorectal mucosa adjacent to CRC, 72 specimens of colorectal adenoma, and 125 specimens of colorectal carcinoma. Results In normal colorectal mucosa, APE1 was detected in nuclei of epithelial cells. Shift of APE1 from nucleus to cytoplasm was observed in 6 of 60 (10%) specimens of mucosa adjacent to cancer. Such shift was observed in 92 of 125 (73.6%) CRC tissues and 60 of 72 (83.3%) colorectal adenoma, the incidence of both of them was significantly higher than that observed in normal colorectal mucosa and colorectal mucosa adjacent to CRC (P