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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Mol Cancer Ther. 2017 Apr 4;16(8):1445–1455. doi: 10.1158/1535-7163.MCT-16-0867

Figure 5. Targeting KRAS versus MYC in Pancreatic Xenograft Tumors.

Figure 5

A, Nude mice harboring PANC-1 xenograft tumors were treated 3 times with 30 μg iRGD-Control (n=2), iRGD-KRAS3 (n=4), or iRGD-MYC2 (n=4) adaptors. Tumor protein lysates were probed for KRAS (left) and MYC (right) expression. Actin served as a loading control. B, Cleaved caspase 3 and C, Ki67 immunofluorescence staining of tumors treated as in A. Three fields at 200X were quantitated for total cell number (DAPI, blue) and FITC-positive cells (B, cleaved caspase 3, green; C, Ki67, green). Statistical significance was calculated by student’s t-test. D, Nude mice harboring PANC-1 xenograft tumors were treated 5 times over 17 days with HEPES buffer or 30 μg iRGD-Control (n=7), iRGD-KRAS3 (n=7), or iRGD-MYC2 (n=7) adaptors. Tumor size was measured and plotted at each treatment day. Statistical significance was calculated by student’s t-test. Scale bar=50 μm