TRAIL-mediated apoptosis in malignant glioma cells is augmented by celecoxib through proteasomal degradation of survivin
Section snippets
Acknowledgements
This work was supported by grants from the Post-Doc Program of the University of Heidelberg to Dr. med. Markus David Siegelin. The plasmid pcDNA3-survivin was kindly provided by Dr. Dario Altieri.
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2013, International Review of Cell and Molecular BiologyCitation Excerpt :This appears to at least partially involve transcriptional regulation of survivin at the − 75/− 66-bp region and the Wnt/beta-catenin signaling pathway (Sakoguchi-Okada et al., 2007). Other studies also suggest that inhibition of survivin expression may involve celecoxib-activated p38 MAPK (Hsiao et al., 2007) or celecoxib-mediated proteasomal degradation of survivin protein (Gaiser et al., 2008). Additionally, OSU-03012, a novel celecoxib derivative and a known PDK-1 inhibitor, was shown to downregulate survivin and XIAP but not Bcl-2 (Zhang et al., 2007), likely by inhibiting upstream signaling pathways (Jak/Stat3, ERK1/2).
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2010, Journal of Investigative DermatologyCitation Excerpt :COX-2 overexpression also conferred resistance to TRAIL-induced apoptosis in colon cancer cells (Tang et al., 2002). Enhancement of TRAIL-induced apoptosis has been shown for celecoxib in glioma cells as well as in prostate, colon, and lung cancer cells (Liu et al., 2006; Chen et al., 2007; Gaiser et al., 2008; He et al., 2008). In pancreatic carcinoma and hepatoma cells, COX-2 inhibitors were also shown to increase CD95L sensitivity (Dauer et al., 2005; Kern et al., 2006).
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