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. Author manuscript; available in PMC: 2017 May 31.
Published in final edited form as: Mol Cancer Res. 2017 Feb 9;15(3):250–258. doi: 10.1158/1541-7786.MCR-16-0132

Figure 2.

Figure 2

Sunitinib induces autophagic flux in CCOC cells. A, CCOC cells were treated with sunitinib for 48 hours, and p62 and LC3 protein levels were assessed. Actin served as a loading control. Bar graphs show the average ± SD (n = 3; one-way ANOVA plus a Dunnet posttest). B and C, CCOC cells were cultured under normoxia (B) or hypoxia (C) and treated with 2.5 or 5 μmol/L sunitinib for 48 hours in the presence or absence of saturating concentrations of Lys05. n.s., not significant. Actin or GAPDH served as a loading control. Bar graphs, average ± SD (n = 3–5; one-way ANOVA plus a Dunnet posttest). D, CCOC cells were serum starved for 24 hours, followed by the addition of serum in the presence or absence of the indicated concentrations of sunitinib for 1 hour. The phosphorylation status of mTOR and S6 ribosomal protein is shown (n = 3). GAPDH served as a loading control.*, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001. Sut, Sutent.