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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Cancer Gene Ther. 2015 Sep 25;22(10):496–505. doi: 10.1038/cgt.2015.49

Figure 4. ASCL1 suppression inhibits BON cell proliferation and CgA expression.

Figure 4

Treatment with an ASCL1-specific siRNA resulted in an inhibition in BON cell proliferation over a 6 day period. A MTT cell viability assay was performed every 2 days, and optical densities were normalized to values starting from the day of transfection. No effect was observed on cell proliferation among cells treated with the nonspecific-siRNA (NS-siRNA) relative to cells treated with Lipofectamine 2000® alone (no siRNA). Data is graphed ± SEM (*p<0.05) (A). Cell lysates were harvested every 2 days and Western blotting was performed to assess the degree of ASCL1 knockdown. Protein expression of ASCL1 was continuously suppressed over the 6 day period while still present in cells treated with the NS-siRNA or Lipofectamine 2000® alone (B). BON cells were treated with ASCL1-siRNA at concentrations ranging from 5nM to 40nM to achieve a steady reduction in ASCL1 expression. Western blotting revealed that CgA levels directly correlated with ASCL1 levels as they were progressively diminished alongside incremental ASCL1 depletion. Once again, the NS-siRNA treated group (NS) did not experience any change in ASCL1 or CgA levels (C).