【Objectives】 To explore the function of PTEN gene in the PI3K/AKT pathway

to evaluate the function of PTEN gene in the antitumor therapy. 【Methods】 Two lentiviral vectors were constructed: one was used to conduct the RNA interference against PTEN gene

another was used to over-express the wild type PTEN gene. These two vectors were transducted into the two endometrial cancer cell lines with different PTEN status. Cell viability was evaluated by MTT assay. Cell apoptosis and cell cycle were evaluated by flow cytometry. Western blotting was performed to evaluate the related protein alteration in PI3K/AKT signaling pathway after the cell transfection. 【Results】1.When PTEN was knocked down with siRNA on HEC-1A cells (PTEN wild type)

there was no significant change in both cell viability and cell apoptosis rate compared with HEC-1A cells. On Ishikawa cells (PTEN mutated)

when PTEN gene was over-expressed

the results of cell viability and cell apoptosis rate showed cell proliferation was inhibited obviously; 2.Western blot results demonstrated that PTEN expression in HEC-1A-RNAi cells was abated

expression of EGFR

p-EGFR

mTOR

p-mTOR

AKT

p-AKT were up-regulated

PI3K/AKT pathway was activated. In Ishikawa-PTEN cells with PTEN over-expressed

the results manifested that expression of EGFR

p-EGFR

mTOR

p-mTOR

AKT

p-AKT were down-regulated

PI3K/AKT pathway was inhibited. 3.When PTEN was knocked down

the proportion of cells in G1 phase decreased and the proportion of cells in S phase increased. By contrast

when PTEN over-expressed

the proportion of cells in G1 phase increased and the proportion of cells in S phase decreased.【Conclusions】 PTEN genes can restrain cell proliferation process

might become one of the choices in endometrial carcinoma gene therapy.