Increase the expression of miR-378 by eicosapentaenoic acid to inhibit Prostate cancer cell proliferation

• Main Authors: Ching Lung Liu, 劉慶隆
• Other Authors: 翁文慧
• Format: Others
• Language: zh-TW
• Published: 2018
• Online Access: http://ndltd.ncl.edu.tw/handle/3d35he

碩士 === 國立臺北科技大學 === 化學工程與生物科技系生化與生醫工程碩士班 === 106 === Prostate cancer is the second most common cancer in the world, and one of the most common malignancies in men. Regard to the advanced prostate cancer, one tumor metastasis hormone therapy is supposed as the best treatment. However, patients will die due to drug resistance eventually. Recently many studies have shown that microRNAs are highly related to the tumor growth. Our previous studies have confirmed that increasing miR-378 expression can significantly inhibit tumor cell proliferation, and improved the targeted drug sensitivities in colorectal cancers. Similarly in prostate cancer, miR-378 also shows low expression in the cells, and it is extremely important in the AKT signaling pathway, prostate cancer is highly correlated to the kallikrein family. As known that miR-378 target-related genes include KLK2, KLK4 and KLK14, which indirect regulation of androgen receptors, and therefore can achieve inhibitory effects to the cells. The hypothesis of this studies, to increase the expression of miR-378 in prostate cancer, will then suppress the expression of the KLK family further to inhibit tumor proliferation. The aim of current study, stimulate the transcription of genes in prostate cancer cells through EPA to increase the expression of miR-378, it will further inhibit the proliferation of tumor. The method, we increased the expression of miR-378 by directly transfecting to the prostate cancer cell lines (CWR22R, DU145, LNCaP, PC3) and indirectly induced by EPA, and observed the related protein expression by western blot. The results show that the protein expression of KLK2 and KLK4 can be observed by transfection and the EPA induced cell lines. We concluded that the cell proliferation can be inhibited through the increasing of miR-378 expression. Hopefully, our finding will provide the clinical treatment another optivied choice.