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Figure 3 | Molecular Cancer

Figure 3

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 3

Effects of Vav3 siRNA (si-Vav3) and docetaxel (DTX) on apoptosis and Bcl-2, Bad, and AR activation in LNCaPH cells. A, B, C and D, si-Vav3 in the presence or absence of DTX induced apoptosis in LNCaPH cells, as detected and quantified by flow cytometry and DNA fragmentation. Note the percent of apoptotic cells with sub-G1 DNA content and fold increase in DNA fragmentation. LNCaPH cells were treated with or without si-Vav3 in the presence or absence of 5 nM DTX for the indicated times (A) or DTX at the concentrations of 0, 1, 2.5, and 5 nM for 72 h (B). Values represent the mean ± SE of three independent experiments. Asterisk indicates P <0.05 compared with LNCaPH cells treated with DTX alone. C, change in the cell cycle distribution in response to si-Vav3 in the presence or absence of DTX for 72 h. D, detection of apoptotic cells using Cell Death Detection ELISAPLUS following 24-h treatment with si-Vav3 in the presence or absence of 5 nM DTX. Values represent the mean ± SE of three independent experiments. Asterisk indicates P < 0.05 compared with LNCaPH cells treated with DTX alone. E, caspase-9 and caspase-3 activation and PARP cleavage after treatment with si-Vav3 in the presence or absence of DTX for 72 h. Blots were stripped and reprobed with an antibody against β-tubulin. LNCaP cells were treated with 10 nM DTX (a known apoptosis inducer) for 72 h as a positive control for apoptosis. F, Bcl-2, Bad, and AR phosphorylation induced by si-Vav3 in the presence or absence of DTX was determined by immunoblot analysis using phospho-Bcl-2 (Ser 70), phospho-Bad (Ser 112), and phospho-AR (Ser 81) antibodies. Blots were stripped and reprobed with antibodies against total Bcl-2, total Bad, total AR, and β-tubulin.

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