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. Author manuscript; available in PMC: 2013 Nov 1.
Published in final edited form as: Mol Cancer Ther. 2012 Sep 18;11(11):2311–2320. doi: 10.1158/1535-7163.MCT-12-0009

Figure 6. STAT3 activation is impaired in PTK6 knockdown cells following DNA damage.

Figure 6

(A) HCT116 p53+/+ cells containing empty vector shRNA (V) or one of two different shRNAs (49, 52) that target PTK6 were treated with either DMSO or 5 or 10 μM of doxorubicin (Dox) and harvested 24 hours post treatment. Immunoblotting was performed using antibodies against PTK6, Phospho-AKT, Total AKT, Phospho-ERK1/2, Total ERK1/2, Phospho-ERK5 and Total ERK5. β-actin was examined as a loading control. (B) HCT116 p53+/+ cells containing empty vector shRNA (V) or shRNAs (49, 52) were treated with either DMSO or 5 or 10 μM of doxorubicin (Dox) and harvested 24 hours post treatment. Immunoblotting was performed using antibodies against PTK6, Phospho-STAT3 and Total STAT3. β-actin was examined as a loading control. (C) Immunoblot analysis of lysates from wild type (+/+) and Ptk6 −/− YAMC cells that were untreated or exposed to 20 Gy of γ-irradiation and harvested 48 hours post treatment. Immunoblotting was performed using antibodies against p53, p21, phospho-STAT3, total STAT3 and cleaved Caspase 3. β-actin was examined as a loading control.