Tat enhances vIL-6-induced angiogenesis and tumorigenesis through inactivation of PTEN and GSK-3β signals in CAM model.

<p>(<b>A</b>) Overexpression of PTEN suppressed the enhanced effect of Tat on vIL-6-mediated angiogenesis. 4E3 cells were transfected by pPTEN and its control plasmid pcDNA for 24 hours and followed by Tat or Mock transduction for another 24 hours. Collected cells were implanted onto the CAM. The quantification of blood vessels was expressed as the mean ± SD (n = 5 to 8). Two independent experiments were performed with similar results. (<b>B</b>) Overexpression of PTEN suppressed the enhanced effect of Tat on vIL-6-mediated angiogenesis. 4E3 cells were treated as in (A). Quantification of tumor weight was expressed as the mean ± SD (n = 5). (<b>C</b>) Overexpression of PTEN restrained the enhanced effect of Tat on phosphorylation of AKT and GSK-3β by vIL-6. 4E3 cells were treated as in (A). Collected cells were implanted onto the CAM. The phosphorylation levels of AKT and GSK-3β in tumor tissues of the CAM model were analyzed by Western blot. (<b>D</b>) Overexpression of GSK-3β decreased the promoted effect of Tat on vIL-6-mediated angiogenesis. 4E3 cells were transfected by the pS9A and its control plasmid pcDNA for 24 hours and followed by Tat or Mock transduction for another 24 hours. Collected cells were implanted onto the CAM. The quantification of blood vessels was expressed as the mean ± SD (n = 5 to 8). (<b>E</b>) Overexpression of GSK-3β decreased the promoted effect of Tat on vIL-6-mediated tumorigenesis. 4E3 cells were treated as in (D). Quantification of tumor weight was expressed as the mean ± SD (n = 5).