Dioscin sensitizes cells to TRAIL-induced apoptosis through downregulation of c-FLIP and Bcl-2
- Authors
- Kim, Yong-Sik; Kim, Eun-Ae; Park, Kyu-Gun; Lee, Sung-Jun; Kim, Mi-Sun; Sohn, Ho-Yong; Lee, Tae-Jin
- Issue Date
- Nov-2012
- Publisher
- Demetrios A. Spandidos Ed. & Pub.
- Keywords
- dioscin; tumor necrosis factor-related apoptosis-inducing ligand; c-FLIP; Bcl-2
- Citation
- Oncology Reports, v.28, no.5, pp 1910 - 1916
- Pages
- 7
- Journal Title
- Oncology Reports
- Volume
- 28
- Number
- 5
- Start Page
- 1910
- End Page
- 1916
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/14727
- DOI
- 10.3892/or.2012.1962
- ISSN
- 1021-335X
1791-2431
- Abstract
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has received attention as a potential anticancer drug, because it induces apoptosis in a wide variety of cancer cells but not in most normal human cell types. Here, we showed that co-treatment with subtoxic doses of dioscin and TRAIL-induced apoptosis in Caki human renal cancer cells. Treatment of Caki cells with dioscin downregulated c-FLIPL and Bcl-2 proteins in a dose-dependent manner. Dioscin-induced decrease in c-FLIPL protein levels may be caused by the increased protein instability. We also found that dioscin induced downregulation of Bcl-2 at the transcriptional level. Pretreatment with NAC slightly inhibited the expression levels of c-FLIPL downregulated by the treatment of dioscin, suggesting that dioscin is partially dependent on the generation of ROS for downregulation of c-FLIPL. Taken together, the present study demonstrates that dioscin enhances TRAIL-induced apoptosis in human renal cancer cells by downregulation of c-FLIPL and Bcl-2.
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Collections - College of Medicine > Department of Microbiology > 1. Journal Articles
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