The effect of Emodin on MIR-25 expression in HT-29 human colorectal cancer cell line

Cancer is characterized by uncontrolled cell division, inactivation of apoptosis, metastasis, and development of angiogenesis depending on abnormal gene expressions. Compared with other types of cancer, colorectal cancer is at the top considering mortality. Many compounds which have anticancer properties are widely used. Emodin (1,3,8-trihidroksi-6-metilantraquinon), which is located into root and rhizome of Rheum species and is an active compound for anthraquinone, exhibits obstructing tumor growth. For this purpose, many chemicals affecting gene expression and their impact mechanisms are enlightened in cancers related closely to modifications of cell gene expressions. Another crucial molecule is micro RNA (miRNA) for organizing gene expression. Differences of miRNA expression in various cancer types are linked with some cellular mechanisms. MicroRNA-25 (miR-25) takes charge as both oncogene and tumor suppressor in cells. In this study, we aimed to investigate the effect of emodin on miR-25 expression in HT-29 which is a cell line of colorectal cancer. For this purpose, we used cell culture to determine duration and dose of chemicals for cell proliferation and apoptosis. Then, we assessed expression of miR-25. As a result of the data, IC50 and AP50 were determined as 55 μM. There is no effect of emodin on the cyclin D1 in the cell cycle. Emodin increases expression of miR-25 and also induces apoptosis by suppressing the expression of survivin.