Disruption of Stat3 reveals a critical role in both the initiation and the promotion stages of epithelial carcinogenesis
J. Clin. Invest. Keith Syson Chan, et al. 114:720 doi:10.1172/JCI21032 [
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Figure 5Effects of a Stat3 decoy oligonucleotide on growth of initiated keratinocytes in vitro and in vivo. (
A) Effect of vehicle control (TE), mutant oligonucleotide control, and Stat3 decoy oligonucleotide on growth of
v-Ha-ras–transduced keratinocytes 48 hours after treatment. Scale bar: 100 μm. (
B) Western blot analysis of Stat3, Bcl-x
L, and cyclin D1 levels in v-Ha-ras keratinocytes treated with vehicle control (con), mutant decoy (mut), or Stat3 decoy (decoy) for 48 hours. (
C) Effect of mutant oligonucleotide control (left 2 mice) and Stat3 decoy oligonucleotide (right 3 mice) on TPA-induced papilloma formation in TG.AC mice at 6 weeks and 13 weeks after first TPA treatment. Arrows indicate papillomas developing in TG.AC mice that received the mutant oligonucleotide together with TPA. (
D) Immunohistochemical stain of PYStat3 in a representative section from a skin papilloma. Scale bar: 25 μm. (
E) Immunohistochemical stain of Ki67 in a representative section of a skin papilloma. Scale bar: 25 μm. (
F) Effect of mutant oligonucleotide and Stat3 decoy oligonucleotide on growth of primary skin papillomas after 2 weeks of treatment. Arrows, tumors injected with mutant oligonucleotide; arrowhead, tumor injected with Stat3 decoy.
