To discuss the treatment of fatty acid induced expression of miR-378 by mouse model.

• Main Authors: Cheng-Chi Wang, 王政祺
• Other Authors: Wen-Hui Weng
• Format: Others
• Language: zh-TW
• Online Access: http://ndltd.ncl.edu.tw/handle/f5d7xe

碩士 === 國立臺北科技大學 === 生化與生醫工程研究所 === 104 === In previous study, we have showed that the expression of microRNA-378 (miR-378) in KRAS and BRAF are low in mutant colorectal cancer (CRC), but not in wild type CRC. Moreover, we also successfully transfected miR-378 into mutated CRC cells. Our data demonstrated that increase expression level of miR-378 in mutant CRC cells could restore the sensitivity of target drug. In addition, miR-378 located on 3’ end of PGC-1β gene and miR-378 expression level could be enhanced via simulated PGC-1β gene by using EPA. Herein, we conducted in vivo test based on our previous study, to further understand the role of miR-378 in living organism and the value of clinical treatment applications. Next, we referred to the recommended dose of EPA, combined with target drug in mouse model for further clinical therapeutic application and proved the expression of miR-378 could be enhanced by EPA. Finally, we detected cells response rate to the target drug, and monitor tumor progression. We use western blotting to detect the expression of p-eIF2. The results demonstrated that expression level of p-eIF2 could be increased via transfecting of miR-378. In animal experiment, we observed that sensitivity of the target drug could be improved by using EPA, and inhibit tumor growth. We expect the result will provide more than 40% treatment benefit of CRC patients, whose tumors contain with mutant KRAS or BRAF genes were considered resistant to the target drug and only can receive conventional therapies and it will provide a great helpful to clinical treatments.