Auricularia auricula increases an apoptosis in human hepatocellular carcinoma cells via a regulation of the peroxiredoxin1

细胞凋亡 细胞培养 癌细胞 肝细胞癌 MTT法 肝癌 超氧化物歧化酶 癌症研究 氧化应激 癌症 细胞 G2水电站 细胞生长 分子生物学 生物 生物化学 遗传学
作者
Mi Ae Kang,Young Keul Jeon,Myeong Jin Nam
出处
期刊:Journal of Food Biochemistry [Wiley]
卷期号:44 (10) 被引量:13
标识
DOI:10.1111/jfbc.13373
摘要

Auricularia auricula (A. auricula) has been reported to have positive health effects. Therefore, this study was conducted to explore possible mechanisms of A. auricula-induced anticancer activity in hepatocellular carcinoma (HCC) cells. First, using proliferative assay including MTT assay and real-time cell electronic sensing technique, we founded that A. auricula has an antiproliferative effect on various cancer cell lines. Among five cancer cell lines, we focused on huh-7 cell line, HCC cell line, due to that A. auricula has most dramatic antiproliferative effects on huh-7 cell line. Following experiments, we founded that its antiproliferative effects was related with apoptosis-inducing activities. For more investigation, a two-dimensional electrophoresis based-proteomic analysis (2DE-GE) was employed for identification of possible target-related proteins of A. auricula-induced apoptosis. Among seven identified proteins, we focused on peroxiredoxin1 (PRDX1), which has been known as an anti-oxidative enzyme. We confirmed downregulation of expression of PRDX1 following A. auricula treatment in mRNA and protein level. In order to obtain a more validation of the correlation of A. auricula-induced cell death and anti-oxidative enzyme. We investigated the level of anti-oxidative enzymes, total glutathione (GSSG/GSH), and superoxide dismutase (SOD) levels in treated cells and PRDX1 gene-silenced cells. GSH and SOD levels were decreased in the treated cells and PRDX1 gene-silenced cells. Our findings suggest that A. auricula is a potent inducer of apoptosis in HCC cells via PRDX1-inhibition pathways. Practical applications Hepatocellular carcinoma (HCC) is among the leading causes of cancer-related mortality. The principal treatment is surgical resection or liver transplantation. However, in most patients with HCC the diagnosis is often late, thereby excluding the patients from definitive surgical resection. Chemotherapy and radiotherapy are generally ineffective. Newer treatments are needed with several being in development. In this research article, we provide regulation mechanism of PRDX1 in HCC. PRDX1 has a proliferative effect and play a role in cancer development or progression. Overexpression of PRDX1 in cancer cells implies the role of PRDX1 in the cancer therapy. PRDX1 is currently being investigated as a new target for gene therapy in cancer. A. auricula is an apoptotic inducer of HCC cells through PRDX1 pathway. Regulation of PRDX1 in HCC may contribute to cancer treatment. Therefore, the potentials of targeting apoptosis would be a viable therapeutic strategy to improve the outcome of HCC patients.
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