Galangin sensitizes TRAIL-induced apoptosis through down-regulation of anti-apoptotic proteins in renal carcinoma Caki cells.
- Affiliated Author(s)
- 김신; 박종욱; 권택규
- Alternative Author(s)
- Kim, Shin; Park, Jong Wook; Kwon, Taeg Kyu
- Journal Title
- Scientific Reports
- ISSN
- 2045-2322
- Issued Date
- 2016
- Abstract
- Galangin, bioflavonoids, has been shown anti-cancer properties in various cancer cells. In this study,
we investigated whether galangin could enhance TRAIL-mediated apoptosis in TRAIL resistant renal
carcinoma Caki cells. Galangin alone and TRAIL alone had no effect on apoptosis, while combined
treatment with galangin and TRAIL significantly induced apoptosis in renal carcinoma (Caki, ACHN and
A498) but not normal cells (normal mouse kidney cells and human normal mesangial cells). Galangin
induced down-regulation of Bcl-2 protein at the transcriptional level via inhibition of NF-κB activation
but not p53 pathway. Furthermore, galangin induced down-regulation of cFLIP, Mcl-1 and survivin
expression at the post-translational levels, and the over-expression of Bcl-2, cFLIP, Mcl-1 and survivin
markedly reduced galangin-induced TRAIL sensitization. In addition, galangin increased proteasome
activity, but galangin had no effect on expression of proteasome subunits (PSMA5 and PSMD4). In
conclusion, our investigation suggests that galangin is a potent candidate for sensitizer of TRAIL
resistant cancer cell therapy.
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