Objective: PI3K/AKT signal pathway is important for negative regulation of FoxO3a/p27Kip1, maintaining cell survival and inhibiting apoptosis. Phosphatase and tensin homology deleted on chromosome 10 (PTEN) gene negatively regulates PI3K/AKT signal pathway. It's downregulation is correlated with prostate cancer (PC) pathogenesis. Previous study showed significantly elevated miR-26a expression in PC tissues, indicating its tumor facilitating role in PC. Bioinformatics analysis revealed targeted relationship between miR-26a and 3'-UTR of PTEN mRNA. This study investigated if miR-26a and PTEN dysregulation played a role in proliferation and apoptosis of PC-3 cells. Materials and Methods: PC tumor tissues were collected along with benign prostate hyperplasia samples. Expression of miR-26a and PTEN was detected. The targeted relationship between miR-26a and PTEN was analyzed by dual-luciferase reporter gene assay. In vitro-cultured PC-3 cells were treated with miR-26a inhibitor and/or pIRES2-PTEN. Flow cytometry was employed to detect cell apoptosis, cycle, and Ki-67 expression. Expression of miR-26a and PTEN was analyzed. Western blot was employed to detect protein levels of p-AKT, p-FoxO3a, and p27Kip1. Results: PC tissues had elevated miR-26a expression and lower PTEN expression compared with benign hyperplasia. miR-26a targeted and inhibited PTEN expression. Transfection of miR-26a inhibitor and/or overexpression of PTEN significantly decreased phosphorylation activity of AKT and FoxO3a, enhanced p27Kip1 expression, cell apoptosis, weakened proliferation ability, and arrested cell cycle at G0/G1 phase. Conclusions: PC tissue had higher miR-26a and lower PTEN expressions. miR-26a targeted and inhibited PTEN, potentiated phosphorylation activity of AKT and FoxO3a, downregulated p27Kip1 expression, decreased cell apoptosis, and facilitated proliferation.

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