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. 2012 Feb 15;7(2):e31070. doi: 10.1371/journal.pone.0031070

Figure 5. Tumor inhibition in mouse model, and effects on EGFR expression and Akt phosphorylation.

Figure 5

(5a) Tumor growth inhibition in mice. MDA-MB-468 subcutaneous breast tumors treated systemically with P/AON/2C5, or P/AON/2C5/TfR were significantly inhibited compared with PBS (control), P(polymer only), or P/2C5 (without anti-tumor component) (P<0.03). The highest inhibition of tumor growth was observed in mice treated with P/AON/2C5/TfR (p<0.03 vs. controls; p<0.05 vs. P/AON/2C5). Error bars denote SEM. (5b) Expression of EGFR and phosphorylated Akt (p-Akt) after treatment of EGFR-positive tumors in vivo. Western blot analysis showed the decrease in EGFR and p-Akt expression in P/AON/2C5-, or P/AON/2C5/TfR -treated mice compared to controls. The highest inhibition of EGFR and p-Akt was seen upon treatment with P/AON/2C5/TfR where 2 targeting antibodies were combined. GAPDH was an internal control to normalize gel loading. (5c) Histopathological analysis of tumors. Hematoxylin and eosin staining of tumors treated with PBS, P, P/2C5, P/AON/2C5 or the leading drug P/AON/2C5/TfR. Consistent with tumor size reduction data, the leading drug P/AON/2C5/TfR treated tumor showed significant reduction in the number of viable tumor cells as compared to other treatments.