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. Author manuscript; available in PMC: 2010 Sep 2.
Published in final edited form as: Cancer Biol Ther. 2008 Dec 11;7(12):1994–2003. doi: 10.4161/cbt.7.12.6967

Figure 4.

Figure 4

VEGFR2 or Src inhibition abrogates STAT3 activation by VEGF. HUVEC were cultured in medium containing 0.5% serum for 24 hours and exposed to different concentrations of SU5416, PP1 or PP2 inhibitor for one hour. VEGF (10 ng/mg) was added, and cell lysates were prepared 10 minutes later. Western blots of lysates from cells treated with SU5416, a VEGFR2 inhibitor, were probed with antibodies to p-VEGFR2, p-Src and p-STAT3; the last blot was stripped and reprobed with antibody to STAT3 (A). Blots of lysates from cells treated with c-Src inhibitors PP1 (B) or PP2 (C) were probed with antibodies to p-Src and p-STAT3; these blots were stripped and reprobed with antibodies to Src and STAT3, respectively. All experiments were performed twice with similar results.