| Summary: | 碩士 === 中山醫學大學 === 生化暨生物科技研究所 === 97 === Since 1982, cancer is the leading cause of deaths in Taiwanese and lung cancer contributes the main death among the cancers. Approximately 40% of lung cancers are adenocarcinomas, and the others are 30 % of Squamous cell carcinoma and 10% of large cell carcinoma and 20% of Small cell carcinoma.In clinic, lung cancer is hard to cure and control with the current treatments, such as surgery resection, chemotherapy and radiotherapy, which frequently cause undesirable and adverse side effects. Recently, mounting evidences reveal that use of medicinal plants may be regarded as a supplement with good efficacy and few side effects for the current cancer treatment. Among the medicinal plants, Ocimum gratissimum Linn has been extensively used in Taiwan. Ocimum gratissimum Linn has been reported to show anti-oxidant, anti-carcinogenic and anti-fibrosis therapeutic effects. However, the underlying antitumor mechanism of Ocimum gratissimum Linn against lung cancer still remains unclear. Here we aimed to investigate the effects of aqueous extract of OG leaf (OGE) on malignant lung cancer cell line A549. Our results revealed that OGE dose -dependently decreased the cell viability of A549. Further investigation showed that OGE suppressed the expression of Bcl-2 and the activation of caspase-9, caspase-8 and caspase-3, which may synergistically induce the apoptosis of A549. Additionally, OGE treatment was found to increase the phosphorylation of p38 and JNK but decrease the phosphorylation of ERK. Proteomic approach, using two-dimensional gel electrophoresis (2-DE) and MALDI-MS analysis, revealed that OGE treatment led to a differential protein expression profile as comparing with mock control. Among the protein spots with differential expression on 2-D gel, 14 spots were further in-gel digested and identified by peptide-mass fingerprint (PMF). The identified proteins including Heat shock protein, peroxiredoxin-1, triosephosphate isomerase, NADH dehydrogenase, actin, SLC15A3 protein, retinal dehydrogenase 1 and malignant T cell amplified sequence 1. In conclusion, our findings indicate that OGE effectively induce the apoptosis of A549 cell through the mitochondrial apoptotic pathway and the activation of p38 and JNK mitogen-activated kinase pathway. Further proteomic analysis reveals that OGE treatment results in a different protein expression pattern; however, the proteins showing differential level still need further investigation and biological validation for mining potential biomarkers.
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