UA inactivated Akt/ERK signaling to inhibit cell proloferation.

<p>(<b>A, B</b>)<b>,</b> SW480 cells were treated with UA at 20µM or 40 µM for 48 h. The expression of the phosphorylated or total PI3K, Akt, mTOR, PTEN, JNK, ERK1/2 proteins was detected by Western blot. GAPDH was used as a control for sample loading. (<b>C, D</b>)<b>,</b> SW480 cells were treated with a PI3K/Akt-selective inhibitor LY294002 (LY, 5 µM) (<b>C</b>) or with an ERK-selective inhibitor U0126 (20 µM) (<b>D</b>) for 4 hours, and then treated with UA at 20 µM. At 48 hours after treatment, cell viability was determined by MTT analysis. The percent cell viability in each treatment group was calculated relative to cells treated with the vehicle control DMSO. The data are presented as the mean ± SD of three separate experiments. *, <i>P</i><0.05, significant differences between treatment groups and control groups.