| Summary: | 碩士 === 中國醫藥大學 === 癌症生物學研究所碩士班 === 101 === In general, patients suffered from advanced hepatocellular carcinoma can be treated only by target therapy, while their survival rate is still a few months more than that with conventional therapy. In order to develop better new drugs to against hepatocellular carcinoma, we screened a variety of compounds and treated different concentrations of drugs in four human hepatocellular carcinoma (HCC) cells, and then examined cell viability by MTT assay. Results show that the acriflavine (ACF) suppressed the viability of HCC cell lines in a dose-dependent manner. Flow cytometry analysis reveals that ACF induced largely the accumulation of Sub-G1 population of Mahlavu cells. Moreover, ACF decreased the expression of Bcl-2 and the activation of caspase-3. The content of cleaved PARP-1 was significantly increased. These findings suggest that ACF could suppress HCC cell growth through caspase-3 activation pathway. In comparing to sorafenib, the IC50 of ACF (1 μM) was nearly tenfold lower than that in sorafenib (13 μM). In vivo test, nude mice received subcutaneously Mablavu cell xenografts and randomly assigned them into two groups, as control and experimental group. Treatment was initiated 3 days after implantation and continued intraperitoneal injection 0.9 % normal saline or 2 mg/Kg of ACF by daily for 5 weeks. Tumors were palpable in vehicle treated mice by day 3 and grew to approximately 2000 mm3 by the end of the experiment, whereas mice treated with ACF experienced tumor growth to approximately 500 mm3. In this study, we confirmed the ACF inhibits cell growth in HCC cells. To expect our results can help to clarify the mechanism of HCC, and the opportunity to provide a clinical treatment guidelines and new target therapy to improve prolong survival with patients of advanced HCC.
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