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. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Cancer Prev Res (Phila). 2011 Aug 31;4(12):2083–2091. doi: 10.1158/1940-6207.CAPR-11-0319

Figure 3.

Figure 3

CPT inhibits VEGFR-3-mediated ERK1/2 pathway. A, B, CPT inhibited phosphorylation of ERK1/2, but not AKT, in LECs in a concentration- and time-dependent manner. LECs treated with CPT (0–10 mM) for 24 h (A) or CPT (10 µM) for 0–24 h (B) were harvested and subjected to Western blot analysis with indicated antibodies. b-tubulin was used as a loading control. C, Overexpression of VEGFR-3 conferred resistance to CPT (10 µM) for 24 h, followed by Western blotting with indicated antibodies. D, Downregulation of VEGFR-3 mimicked the effect of CPT, inhibiting phosphorylation of ERK1/2 in LECs. LECs, infected with lentiviral shRNAs to VEGFR-3 and GFP (control), respectively, were treated with CPT (10 µM) for 24 h, followed by Western blotting with indicated antibodies.