No abstract

It is reported that black raspberry (BRB) anthocyanins could act as a potential chemopreventive agent for colorectal cancer (CRC). However, the underlying mechanism by which BRB anthocyanins inhibits the carcinogenesis of CRC cells has not been elucidated. The abnormal expression of microRNAs (miRNAs) that target important tumor suppressor genes is usually associated with CRC development. In this study, we explored whether BRB anthocyanins could affect the expression of certain miRNAs in an azoxymethane (AOM)/dextran sulphate sodium (DSS)‐induced CRC mouse model and human CRC cell lines. miRNA microarray analysis was used to determine the differences in miRNA expression between AOM/DSS‐induced mice fed with a diet supplemented without or with BRB anthocyanins. The expression of one particular miRNA, miR‐483‐3p, was found to decrease dramatically in AOM/DSS‐induced mice that were fed with a diet supplemented with BRB anthocyanins. Subsequent quantitative real‐time polymerase chain reaction and Western blot analyses showed that the reduced expression of miR‐483‐3p was accompanied by an increased expression of Dickkopf 3 (DKK3), a potential target of miR‐483‐3p as predicted by bioinformatic analysis. The protein and messenger RNA levels of DKK3 were significantly upregulated when the miR‐483‐3p level was reduced by a miR‐483‐3p‐specific inhibitor, suggesting that DKK3 might be the target gene of miR‐483‐3p. In addition, the downstream factors of the DKK3 signaling pathway, which included Wnt/β‐catenin, also played a role in the miR‐483‐3p‐mediated anticancer effect of BRB anthocyanins. Thus, miR‐483‐3p might be a potential target in BRB anthocyanin‐mediated prevention of CRC.

Colorectal cancer (CRC) is a kind of malignant cancer with high morbidity and mortality. The purpose of this study was to explore potential regulated key genes involved in CRC through bioinformatics analysis and experimental verification. The gene expression profile data were downloaded from the Gene Expression Omnibus, and the differential expression genes were detected in cancerous and paracancerous samples of CRC patients, respectively. Then functional enrichment analysis, such as the Kyoto Encyclopedia of Genes and Genomes pathway analysis as well as the protein‐protein interaction network were constructed, and the highly related genes were clustered by Molecular COmplex DEtection algorithm to find out the core interaction in different genes' crosstalk. The genes affecting CRC prognosis were screened by the Human Protein Atlas database. In addition, the expression level of core genes was detected by GEPIA database, and the core genes' changes in large‐scale cancer genome data set were directly analyzed by cBioPortal database. The expression of the predicted hub genes DSN1, AHCY, and ERCC6L was verified by reverse‐transcription quantitative polymerase chain reaction in CRC cells. The gene function of DSN1 was analyzed by wound healing and colony formation assays. The results showed that silencing of DSN1 could significantly reduce the migration and proliferation of CRC cells. Further, BUB1B, the potential interacting protein of DSN1, was also predicted via bioinformatics analysis. Above all, this study shows that bioinformatics analysis combined with experimental method verification provide more potential vital genes for the prevention and therapy of CRC.

No abstract

Taurine has been reported to influence osteogenic differentiation, but the role of taurine on cartilaginous differentiation using human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) remains unclear. In this study, we investigated the effect of taurine (0, 1, 5 and 10 mM) on the proliferation and chondrogenesis of hUC-MSCs by analyzing cell proliferation, accumulation of glycosaminoglycans and expression of cartilage specific mRNA. The results show though taurine did not affected the proliferation of hUC-MSCs, 5 mM of taurine is sufficient to enhanced the accumulation of glycosaminoglycans and up-regulate cartilage specific mRNA expression, namely collagen type II, aggrecan and SOX9. Taurine also inhibits chondrocyte dedifferentiation by reducing expression of collagen type I mRNA. Taken together, our study reveals that taurine promotes and maintains the chondrogenesis of hUC-MSCs.