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. 2011 Aug 31;6(8):e24099. doi: 10.1371/journal.pone.0024099

Figure 3. Expression of putative targets of miR-34a.

Figure 3

(A), Pancreatic CSCs were treated with or without SAHA for 48 h. The expression of acetylated-p53, p21, PUMA, SIRT1, CDK6, CyclinD1, survivin and Bcl-2 was measured by the Western blot analysis. β-actin was used as a loading control. (B), Pancreatic CSCs were treated with or without 5Aza-dC for 48 h. The expression of p21, PUMA, Notch 3, CDK6, survivin and Bcl-2 was measured by the Western blot analysis. β-actin was used as a loading control. (C), SIRT1 3′UTR-Luciferase activity. Pancreatic CSCs were transduced with either SIRT1 3′UTR-Luc construct or SIRT1 mutant 3′UTR-Luc construct, and treated with SAHA (0–3 µM) for 24 h. Luciferase activity was measured as per manufacturer's instructions (Promega). Data represent mean ± SD. *, # or %  =  significantly different from control, P<0.05.