Fig. 2
Docetaxel inhibited HIF-1α-mediated tumor glycolysis. A–B PC-3M IE8 or PC-3M cells were treated with or without docetaxel (5 uM) for 48 h, the level of lactate and glucose in the supernatant were measured according to the instruction. Data represented the mean ± s.d. of three independent experiments and were analyzed by t test for significance versus the control group. **P < 0.01, ***P < 0.001. The total RNA was extracted using trizol reagents, and Real-time PCR was performed to analyze the glycolytic genes expression in PC-3M IE8 (C) and PC-3M cells (D), Data represented the mean ± s.d. of three independent experiments and were analyzed by the one sample t test for significance versus the control group. ***P < 0.001. E Western blotting was employed to detect indicated proteins in PC-3M IE8 and PC-3M cells treated with or without docetaxel for 48 h, α-tubulin served as internal control and the bands intensity were quantified and analyzed by t test for significance versus the control group. Data represented the mean ± s.d. of three independent experiments, **P < 0.01, ***P < 0.001. F PC-3M IE8 cells were treated with docetaxel (5 uM) for 1 h, following by CoCl2 stimulation for further 48 h. The total protein was harvested and detected indicated proteins by SDS-PAGE. A quantification of each blot is indicated. α-tubulin served as internal control, data represented the mean ± s.d. of three independent experiments and analyzed by One-way ANOVA with multiple comparisons, followed by Bonferroni post hoc test for significance. ***P < 0.001