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. 2014 Feb 20;9(2):e89117. doi: 10.1371/journal.pone.0089117

Figure 3. Camptothecin (CPT) upregulates BTG2 expression dependent on p53 response element of the human BTG2 gene in LNCaP cells.

Figure 3

(A) LNCaP cells were treated with indicated concentrations of CPT for 24 hours. Cells were lysed and expressions of BTG2 and p53 were determined by immunoblot assay. (B) Luciferase activity of BTG2 reporter vector (pBTG2-300)-transfected LNCaP cells treated with different concentrations of CPT. (C) Luciferase activity of BTG2 reporter vectors (pBTG2-300) with different concentrations of p53 expression vector-contrasfected LNCaP cells. (D) Luciferase activity of nested deletion or mutation constructs of BTG2 reporter vectors-transfected LNCaP cells after treatment with control solvent (white bars) or 1 µM of CPT (black bars). Data are presented as the mean percentage+SE (n = 6) of the BTG2 reporter activity induce by CPT treatment in relation to the control solvent-treated group (*P<0.05, **P<0.01). LNCaP cells were cotreated with 1 µM CPT and 30 µM pifithrin-α (PFT-α). Cells were lysed and expression of p53 (E) and BTG2 (F) were determined by immunoblotting assay. (G) Luciferase activity of BTG2 promoter vector-transfected LNCaP cells treated with 1 µM of CPT or/and 30 µM PFT-α (*P<0.01).