<p><b>Copyright information:</b></p><p>Taken from "Curcumin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells: molecular mechanisms of apoptosis, migration and angiogenesis"</p><p>http://www.jmolecularsignaling.com/content/2/1/10</p><p>Journal of Molecular Signaling 2007;2():10-10.</p><p>Published online 4 Oct 2007</p><p>PMCID:PMC2082014.</p><p></p>h. Cell viability was measured at the end of 48 h by XTT assay. (B), LNCaP cells were treated with various concentrations of curcumin (0–30 μM) for 24 h, followed by treatment with TRAIL (50 nM) for another 24 h. Cell viability was measured at the end of 48 h by XTT assay. (C), PC-3 cells were seeded in soft agar and treated with curcumin (5–40 μM) in the presence or absence of TRAIL (25 nM). After three weeks, no of colonies were counted. Data represent mean ± SE. (D), LNCaP cells were seeded in soft agar and treated with curcumin (5–40 μM) in the presence or absence of TRAIL (50 nM). After three weeks, no of colonies were counted. Data represent mean ± SE. (E and F), Effects of dominant negative FADD on curcumin and/or TRAIL-induced apoptosis. PC-3 and LNCaP cells were transiently transfected with either control plasmid or plasmid expressing dominant negative FADD (DN-FADD) along with plasmid (pCMV-LacZ) encoding the β-galactosidase (β-Gal) enzyme. There was no difference in transfection efficiency among groups. Transfected cells were treated with curcumin (0, 10 or 20 μM) in the presence or absence of TRAIL (25 nM for PC-3 cells or 50 nM for LNCaP) for 48 h. Apoptosis was measured by DAPI staining. Data represent mean ± SE. * = significantly different from respective control; # and % = treatment groups were significantly different, P < 0.05
