UA activates PTEN to modulate the FAK/PI3K/Akt signaling pathway: (A) Breast cancer cell lines were treated with UA for 48 h. Western blot analysis with antibodies to tumor progression-relevant proteins as indicated. GAPDH was used to normalize the amount of protein in each lane. (B) Incubation of breast cancer cells with UA (30 μM) significantly decreases AGO2. (C) Increased PTEN negatively regulates the expression levels of (D) FAK and (E) PI3-kinase p110 (PI3K), and inactivates the phosphorylated (activated) forms of (F) PI3K (p-P85αTyr467/Tyr199), (G) Akt (p-AktSer473), and (H) mTOR (p-mTOR2481), and reduced level of (I) c-Myc in both cells treated with UA. Densitometric analyzes for Western blot were performed as described in Materials and Methods. Data are shown as mean ± SD for three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001 vs. control group (Ctrl, 0 µM).