Journal
ONCOLOGY REPORTS
Volume 29, Issue 2, Pages 474-480Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2012.2127
Keywords
casticin; apoptosis; cell-surface receptor; tumor necrosis factor-related apoptosis-inducing ligand; colon cancer
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Funding
- Project Item of Scientific Research of the Administration Bureau of Traditional Chinese Medicine of Hunan Province [2010081]
- Project Item of Scientific Research of the Department of Education of Hunan Province [10C0975]
- Major Project Item of Scientific Research of the Department of Education of Hunan Province [09A054]
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We investigated the effect of casticin on apoptosis induced by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). We found that casticin potentiated TRAIL-induced apoptosis in human colon cancer cells. Casticin downregulated cell survival proteins including Bcl-xL, Bcl-2, survivin, XIAP and cFLIP, and induced death receptor 5 (DR5), but had no effect on DR4 and decoy receptors (DcR1 or DcR2). Deletion of DR5 by siRNA significantly reduced the apoptosis induced by TRAIL and casticin. In addition, casticin induced reactive oxygen species (ROS) generation in a dose-dependent manner. Collectively, the present study showed that casticin potentiates TRAIL-induced apoptosis through downregulation of cell survival proteins and induction of DR5 mediated by ROS.
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