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Figure 2 | Molecular Cancer

Figure 2

From: Targeting the Vav3 oncogene enhances docetaxel-induced apoptosis through the inhibition of androgen receptor phosphorylation in LNCaP prostate cancer cells under chronic hypoxia

Figure 2

Effects of Vav3 siRNA (si-Vav3) and docetaxel (DTX) on cell proliferation and Akt, ERK, and JNK activation in LNCaPH cells. A, Vav3 siRNA (si-Vav3) and control scramble siRNA (si-Scr) were added to the medium using a lipophilic transfection-enhancing reagent (Lipofectamine RNAiMAX) in the presence or absence of DTX. Cells were harvested after 72 h, and immunoblot analysis was performed using anti-Vav3 antibody. Blots were stripped and reprobed with an antibody against β-tubulin. B, effects of si-Vav3 in the presence or absence of DTX on the proliferation of LNCaPH cells were determined by cell counting. Values represent the mean ± SE of three independent experiments. Asterisk indicates P <0.05 compared with LNCaPH cells treated with DTX alone. C, live/death viability/cytotoxicity kit assay was used to detect live (green) and dead (red) cells using fluorescence microscopy (4× magnification). D, phosphorylation of Akt, ERK, and JNK induced by si-Vav3 in the presence or absence of DTX was determined by immunoblot analysis using phospho-Akt (Ser 473), phospho-ERK (Thr 202/Tyr 204), and phospho-JNK (Thr 183/Tyr185) antibodies. Blots were stripped and reprobed with antibodies against total Akt, total ERK, total JNK, and β-tubulin. E, phosphorylation levels of Akt, ERK, and JNK in LNCaPH cells were scored as 1.00, and each value is shown as a fold stimulation. Values represent the mean of three independent experiments. Asterisk indicates P < 0.05 compared with LNCaPH.

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