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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Mol Carcinog. 2012 Oct 12;53(3):230–242. doi: 10.1002/mc.21969

Figure 6. AV3 peptide treatment resulted in decreased FAK phosphorylation and decreased VEGFR-3 expression in SK-N-BE(2) cells.

Figure 6

AV3 is a small peptide known to disrupt the binding between FAK and VEGFR-3. Immunoblotting was used to detect FAK and VEGFR-3 phosphorylation and expression following treatment with AV3 or control (TAT) peptide, and immunoblots were analyzed by densitometry. A. In the SK-N-AS cells, AV3 treatment led to little change in phosphorylation of FAK (top blot and middle panel) or total VEGFR-3 (fourth blot and bottom panel) after 24 hours treatment. B. In the SK-N-BE(2) cells, AV3 peptide treatment resulted in a decrease in Y397 FAK phosphorylation (top blot and middle panel), and a decrease in total VEGFR-3 expression after 24 hours (fourth blot and bottom panel). Phosphorylated FAK was presented in relation to total FAK and total VEGFR-3 was presented relative to GAPDH in the densitometry graphs.