Abstract: 【Objective】 Using the preliminary constructed lentivirus and adenovirus blocking or promoting PSMA expression

to explore the relationship between PSMA and PTEN/PI3K/AKT pathway on prostate cancer LNcap cells migration and apopotosis. 【Methods】 The subjects include the stable block PSMA expression in cell lines (interference group)

overexpression of PSMA LNcap cell lines (overexpression group)

without any processing LNcap cell lines (control group). The three groups were cultured in the the general medium and in the medium containing PI3K/Akt pathway inhibitor (LY294002) two environments. Western blot and cellular immune chemical were observed in the three groups of cells about the expression of p-Akt

and CCK-8 assay was used to depict cell growth curve

transwell to detect cell migration

flow cytometry to test apoptosis. 【Results】 Western blot and immunocytochemistry prompted that p-Akt levels decline with the inhibition of PSMA and p-Akt levels improve with the overexpression of PSMA. And the three groups’ p-Akt was at a low level under LY294002 inhibition with no significant differences from each other (P > 0.05). CCK-8 assay showed that the inhibition PSMA leading to the decrease of cell

while overexpression of PSMA leading to the rise. Transwell assay showed that the penetrate cells in control group was 56.30

interfering group was 36.60

and over-expression group was 67.80. Apoptosis rates tested by flow cytometry were 4.7% in interfering group

2.3% in over-expression group and 3.6% in control group. But when LY294002 exist

CCK-8 assay showed that the three groups of cell proliferation were at a low level; transwell assay showed that the penetrated number of cells in each groups had no significant difference between the results without LY294002. Apoptosis rates were 9.3%

3.6% and 4.9% in the three groups. 【Conclusion】 PSMA positively regulates the cell proliferation and apoptosis of LNcap cell line by upregulating the PEN/PI3K/Akt signaling pathway. There must be another pathway which regulated the migration ability induced by PSMA on prostate cancer cell.