Fig. 3.

VEGFR-1/2 contributes to tubulin polymerization. (A) Western blots using a pan α-tubulin polyclonal antibody to probe cell lysates treated with paclitaxel with or without bevacizumab for 24 h during normoxia or hypoxia. Paclitaxel activity was inhibited in hypoxia. Tubulin polymerization was decreased in hypoxia compared with normoxia and it was statistically significant. Cells were treated with paclitaxel with/without bevacizumab at 100 nM and 100 ug/mL, respectively. Lane 1: no drug, 2: paclitaxel, 3: paclitaxel with bevacizumab. Actin was used as a loading control. Band intensities were quantified by densitometry. (B) Hypoxia-dependent upregulation of HIF-1α and TUBB3 was most reversed in the presence of paclitaxel and anti-VEGFR-1 for 24 h. HIF-1α was measured from nuclear fractions, and TUBB3 was measured from total cell lysates. Band intensities were quantified by densitometry. ^*p<0.01. HIF-1α, hypoxia inducible factor-1α; TUBB3, class III β-tubulin; VEGFR, vascular endothelial growth factor receptor.