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. Author manuscript; available in PMC: 2012 Mar 15.
Published in final edited form as: Int J Radiat Oncol Biol Phys. 2011 Jan 13;79(4):1206–1215. doi: 10.1016/j.ijrobp.2010.10.058

Figure 2.

Figure 2

(A) Luciferase assay showing curcumin inhibits IR functionally activated NFκB. SH-SY5Y cells were transfected with pNFκB-Luc and then exposed to 2 Gy with or without Curcumin (100nM). (B) SH-SY5Y cells transfected with pCRE-Luc or pGL3-354 were mock irradiated, exposed to 2Gy or treated with Curcumin and exposed to 2Gy. The transfected cells were further incubated for 24h, and then lysed for the luciferase assay. (C) The ectopic expression of IκBα(S32A/S36A). SH-SY5Y cells were transiently transfected with the indicated plasmid and incubated for 24h. (D) A luciferase reporter assay showing the inhibitory effect of ectopically expressed IκBα(S32A/S36A) on IR-induced transcription of the telomerase gene. Cells co-transfected with either pGL3-354 and a non-specific construct pTAL, or pGL3-354 and pUSEI-IκBα(S32A/S36A), were mock irradiated or exposed to 2Gy. (E) Deleting NFκB binding site on the telomerase promoter attenuates 2Gy induced transcriptional activation. SH-SY5Y cells transfected with mutant (pGL3-347) or wild-type (pGL3-354) construct and incubated for 16h were mock irradiated or exposed to 2Gy. Cells were then harvested at 24h post-irradiation. Data shown represent mean and standard deviation (SD) of three independent experiments. Significant decrease in luciferase activity (P<0.001) in the absence of an intact NFκB binding site.