Figure 1
Glioma-specific and cell cycle-regulated apoptosis mediated by pG8- FasL. (A) The pG8-FasL vector contained three-tandem repeats of the GFAP enhancer element upstream of the minimal CMV promoter to drive glial-specific activation of the transcriptional activator, Gal4/NF-YA. The pG8-FasL amplicon vector consisted of the eGFP gene under the control of the immediate early promoter (IE4/5p) for titering and monitoring of viral infection. (B) pIH8GalFasL was generated by removal of the luciferase gene from pIH8GalLuc (Additional File 1) and replaced with the FasL gene. This vector lacked the Gal4/NF-YA transactivator sequence, and was used as a negative control throughout this study. (C) The percentage of apoptotic cells in pG8-FasL and pIH8GalFasL-transduced ΔGli36 and HeLa cells were analyzed 72 h post-infection. Data shown are the averages of triplicate experiments + SEM. Dotted lines indicate the background apoptosis resulted from the combined effect of lovastatin and low serum level. (D) FasL expression was determined by ELISA in both ΔGli36 and HeLa cells 72 h post-infection. (E) SCID mice harboring either ΔGli36-SCID8 or HeLa were injected with 1× 106 TU of pC8-FasL (purple), pC8-36 (blue), pG8-FasL (red), and pG8-18 (black) vectors. Arrows indicated the repeated injection time. Tumor volume was monitored at different time points.