Curcumin is a polyphenol extracted from turmeric, which that belongs to the Zingiberaceae family. Curcumin has numerous effects, including anti-inflammatory, antitumor, anti-oxidative and antimicrobial effects. However, the effects of curcumin on human breast cancer cells remain largely unknown. The aim of the present study was to investigate the anticancer effects and the mechanisms by which curcumin affects breast cancer cells. The anticancer effect of curcumin on cell viability and cytotoxicity on human breast cancer MCF-7 cells was analyzed using 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide and lactate dehydrogenase assays, respectively. Cell apoptosis of MCF-7 cells was detected using flow cytometry, 4′,6-diamidino-2-phenylindolestaining assay and caspase-3/9 activity kits. Reverse transcription-quantitative polymerase chain reaction was used to analyze microRNA-21 (miR-21) expression in MCF-7 cells. The protein expression of phosphatase and tensin homolog (PTEN) and phospho-protein kinase B (pAkt) was determined by western blot analysis. miR-21 was transfected into MCF-7 cells and the anticancer effect of curcumin on cell viability and the expression of PTEN and pAkt was analyzed. The present results demonstrated that curcumin inhibited cell viability and induced cytotoxicity of MCF-7 cells in a concentration- and time-dependent manner, by inducing apoptosis and increasing caspase-3/9 activities. In addition, curcumin downregulated miR-21 expression in MCF-7 cells by upregulating the PTEN/Akt signaling pathway. The present study has for the first time, to the best of our knowledge, revealed the anticancer effect of curcumin in suppressing breast cancer cell growth, and has elucidated that the miR-21/PTEN/Akt signaling pathway is a key mechanism for the anticancer effects of curcumin.
MicroRNAs (miRs) played important roles in the cell proliferation, apoptosis and other biological processes in cancer. In the present study we found that miR-375 was significantly down-regulated in human papillary thyroid carcinoma (PTC) tissues and cell lines. In this study we try to investigate the biological activity of miR-375 in human PTC cells and try to find the potential target of miR-375. Our study indicated that over-expression of miR-375 could inhibit the PTC cells proliferation and this inhibition was caused by the induction of cell apoptosis. In vivo animal study indicated that over-expression of miR-375 could significantly decrease the migration and invasion of human PTC cell in vivo. These results exhibit over-expression of miR-375 in human PTC cells could inhibit the process of human PTC. Further study demonstrated ERBB2 was a direct target of miR-375, over-expression of miR-375 decrease the both mRNA and protein expression of ERBB2 in human PTC cells. These data indicate miR-375 play important roles in the process and development of human PTC. These finds suggested that appropriate application of miR-375 regulation might be a new sight for the treatment of human PTC in the future.
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