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

Figure 4. Expression of putative targets of miR-34a.

Figure 4

(A), Pancreatic CSCs were transiently transfected with either negative control (scrambled) or anti-miR34a oligonucleotide and treated with Aza-5dC (4 µM) for 48 h. Western blot analysis was performed to measure the expression of cyclin D1, CDK2, p27 and VEGF. β-actin was used as a loading control. (B), Pancreatic CSCs were transiently transfected with either negative control (scrambled) or anti-miR34a oligonucleotide and treated with SAHA (3 µM) for 48 h. Western blot analysis was performed to measure the expression of cyclin D1, CDK2, p27 and VEGF. β-actin was used as a loading control. (C), Regulation of VEGF-B 3′UTR-Luciferase activity by Aza-5dC. Pancreatic CSCs were transfected with either negative control (scrambled) or anti-miR34a oligonucleotides along with VEGF-B 3′UTR-LUC construct, and treated with Aza-5dC (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. (D), Regulation of VEGF-B 3′UTR-Luciferase activity. Pancreatic CSCs were transfected with either negative control (scrambled) or anti-miR34a oligonucleotides along with VEGF-B 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. *, @, #  =  significantly different from control, P<0.05.