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Hispolon from Phellinus linteus induces apoptosis and sensitizes human cancer cells to the tumor necrosis factor-related apoptosis-inducing ligand through upregulation of death receptors

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The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potent anticancer agent possessing the ability to induce apoptosis in various cancer cells but not in nonmalignant cells. However, certain type of cancer cells are resistant to TRAILinduced apoptosis and some acquire resistance after the first treatment. So development of an agent that can reduce or avoid resistance in TRAILinduced apoptosis has garnered significant attention. The present study evaluated the anticancer potential of hispolon in TRAILinduced apoptosis and indicated hispolon can sensitize cancer cells to TRAIL. As the mechanism of action was examined, hispolon was found to activate caspase3, caspase8 and caspase9, while downregulating the expression of cell survival proteins such as cFLIP, Bcl2 and BclxL and upregulating the expression of Bax and truncated Bid. We also found hispolon induced death receptors in a noncell typespecific manner. Upregulation of death receptors by hispolon was found to be p53-independent but linked to the induction of CAAT enhancer binding protein homologous protein (CHOP). Overall, hispolon was demonstrated to potentiate the apoptotic effects of TRAIL through downregulation of antiapoptotic proteins and upregulation of death receptors linked with CHOP and pERK elevation.
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Document Type: Research Article

Affiliations: 1: Department of Biotechnology, Research Institute (RIBHS) and College of Biomedical and Health Science, Konkuk University, Chungju, Chungbuk 27478, Republic of Korea 2: Discovery Research Center, C&C Research Laboratories, Suwonsi, Gyeonggido 440746, Republic of Korea 3: College of Pharmacy, Keimyung University, DalseoGu, Daegu 704701, Republic of Korea

Publication date: February 1, 2016

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