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https://www.selleckchem.com/products/motolimod-vtx-2337.html Background Selenium is a mineral that showed both pro- and anti-oxidant activities in various disease models. In this study, we evaluated the anti-tumor effect of selenium against 1,2-dimethylhydrazine (DMH)-induced colorectal cancer in BALB/C mice and its effect on apoptosis and angiogenesis. Methods Colorectal cancer was induced by subcutaneous injection of DMH (20 mg/kg body weight) in BALB/C mice once weekly for 20 weeks. Selenium (200 mg/L) was given to DMH plus selenium-treated group in the drinking water for the next 3 months. Results The DMH plus selenium-treated group exhibited significantly lower expression of cloned caudal-type homebox gene -2 (CDX-2) and vascular endothelial growth factor (VEGF) but higher caspase-3 expression level at p less then 0.001 compared to the DMH-treated group. Moreover, a decrease in the reduced glutathione content and glutathione peroxidase activity but an increase in the malondialdehyde content were observed at p less then 0.001. Both macroscopic and microscopic examination of the colorectal tissues confirmed the results. Conclusion The anti-tumor effect of selenium against an induced colorectal cancer in mice is attributed to its pro-oxidant, anti-angiogenic and apoptotic effects.Background Abnormal DNA methylation leading to altered transcription of certain genes occurs frequently in colorectal cancer (CRC). As with protein-coding genes, microRNAs (miRNAs) may be targeted for methylation in CRC; however, the methylation state of miRNA genes in CRC, especially in primary lesions, has not yet been completely elucidated. To understand the impact of DNA methylation on the miR-200c/141 cluster promoter, we investigated the methylation and expression of miR-141 in precancerous lesions and colorectal cancer. Methods In this cross-sectional study, 208 colorectal tissue samples, including 34 tumor tissue samples, 60 precancerous lesions with matched normal adjacent tissue

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