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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 4. PTK6 knockdown leads to enhanced apoptosis in HCT116 p53 +/+ cells following treatment with chemotherapeutic DNA-damaging drugs.

Figure 4

(A) HCT116 p53+/+ and 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, p53, p21 cleaved Caspase 3 and cleaved PARP. β-actin was examined as a loading control. (B) HCT116 p53+/+ and p53−/− cells containing empty vector shRNA (V) or one of two different shRNAs (49, 52) that target PTK6 were treated with either DMSO or 300 μM of 5FU and harvested 24 hours post treatment. Immunoblotting was performed using antibodies against PTK6, p53, p21, cleaved Caspase 3 and cleaved PARP. β-actin was examined as a loading control.