| Summary: | 碩士 === 國立臺北科技大學 === 生物科技研究所 === 100 === MicroRNA-378 is a short RNA molecule with 21 base pair that causes gene silencing by the binding of miRNA to their complementary mRNA. Literatures showed low expression of miR-378 correlated with colorectal cancer (CRC). Colorectal cancer is one of the genetic cancers. Cetuximab, a monoclonal antibody, has been used as a target drug for the epidermal growth factor receptor (EGFR) for years. However, when the tumor contain with KRAS or BRAF mutations showed no response to the drug, which account for 40 % and 10 % of CRC patients, respectively. Several binding sites of Mitogen-Activated Protein Kinase (MAPK) pathway were complemented with miR-378 in CRC. We hypothesized transfection of miR-378 into colorectal cancer cell line may suppress the oncoproteins expression of the MAPK pathway. Herein, we using sequencing to identify mutation types of six human colorectal cancer cell line, quantitative RT-PCR to confirmed RNA expression, western blotting to observed oncoproteins expression, then further transfected miR-378 into six CRC cell lines. Our study aimed to observe whether expression level of miR-378 was associated with the oncoproteins in the MAPK pathway. The results showed different level of oncoproteins expression and mutant sites occurred in all cell lines. Transfection of miR-378 reduced the expression level of oncoproteins. The drug test was positive after transfection. This study model provided an important conclusion, the miR-378 can regulate the expression of oncoproteins in MAPK pathway. The influence of cell survival rate and the efficiency of Cetuximab were regulated by miR-378 via suppress protein expression of apoptosis and proliferation in MAPK pathway. The expreesion of ERK protein appears to be a marker for evaluating of miR-378 reduce the cell survival in the future. Our results seem to increase the efficacy of Erbitux after transfected miR-378 in late colorectal cancer cell line.
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