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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Clin Exp Metastasis. 2012 Dec 30;30(5):579–594. doi: 10.1007/s10585-012-9562-5

Figure 6.

Figure 6

Oral administration of PF-271 FAK inhibitor prevents ID8-IP tumor growth and metastasis independent of effects on c-Src Y416 phosphorylation. (A) mCherry-labeled ID8-IP tumor cells were bursal-injected and after 7 days, vehicle or PF-271 (30 mg/kg) were administered by oral gavage twice-daily (BID). Mice were euthanized after 28 days and (A) primary tumor weight was determined for mice treated with vehicle (n=8) or PF-271 (n=10). (B) Peritoneal-associated metastatic tumor sites were quantified by counting mCherry-positive nodules visualized by OV100 imaging. (A and B) Values are means (+/- SD) (* p<0.05, ** p<0.01). (C) Evaluation of FAK Y397 phosphorylation (pY397), total FAK, c-Src Y416 phosphorylation (pY416 Src), total c-Src, and total actin levels by immunoblotting using normal ovary tissue or ID8-IP tumors from 5 independent vehicle- or PF-271-treated mice. (D) Ratio of pY397 phosphorylated FAK to total FAK levels normalized to normal ovary (set to 1) and determined by densitometry using Image J (n= 5 per group, *** p<0.001). (E) Ratio of pY416 phosphorylated c-Src to total c-Src levels normalized to normal ovary (set to 1) and determined by densitometry using Image J (n= 5 per group).