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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Cancer Chemother Pharmacol. 2015 Jan 24;75(4):671–682. doi: 10.1007/s00280-015-2675-1

Figure 5.

Figure 5

(A) Immunohistochemistry of the proliferation marker Ki-67 in A549 tumor sections, (B) western blot of tumor lysate probed for acetylated H3 and H4, (C) western blot of A549 cells treated with Largazole or Largazole analogs. Staining for the Ki-67 proliferative marker (A) in tumor sections is greatly decreased relatively to control in the pyridyl analog depsipeptide, Largazole peptide isostere, and decreased moderately in the pyridyl analog pyridyl disulfide treatment. Western blots of tumor lysates (B) probed with anti-acetylated H3 and H4 show increased acetylation relative to control for all compounds (lane 1 control, lane 2 Largazole, lane 3 Largazole peptide isostere, lane 4 pyridyl analog depsipeptide, lane 5 pyridyl analog peptide isostere, lane 6 pyridyl analog pyridyl disulfide). Dose response of histone acetylation (C) in vitro.