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PTEN  plays an essential role in tumorigenesis and both its mutation and inactivation can influence proliferation, apoptosis, and cell cycle progression in tumor cells. However, the precise role of  PTEN  in lung cancer cells has not been well studied. To address this, we have generated lung adenocarcinoma A549 cells overexpressing wild-type or mutant  PTEN  as well as A549 cells expressing a siRNA directed toward endogenous  PTEN . Overexpression of wild-type  PTEN  profoundly inhibited cell proliferation, promoted cell apoptosis, caused cell cycle arrest at G1, downregulated p-AKT, and decreased expression of the telomerase protein  hTERT . In contrast, in cells expressing a  PTEN  directed siRNA, the opposite effects on cell proliferation, apoptosis, cell cycle arrest, p-AKT levels, and  hTERT  protein expression were observed. A549 cells transfected with a  PTEN  mutant lacking phosphatase activity ( PTEN -C124A) or an empty vector (null) did not show any effect. Furthermore, using the PI3K/AKT pathway blocker LY294002, we confirmed that the PI3K/AKT pathway was involved in mediating these effects of  PTEN . Taken together, we have demonstrated that  PTEN  downregulates the PI3K/AKT/ hTERT  pathway, thereby suppressing the growth of lung adenocarcinoma cells. Our study may provide evidence for a promising therapeutic target for the treatment of lung adenocarcinoma.

biomed research international

<i>PTEN</i>Inhibits Cell Proliferation, Promotes Cell Apoptosis, and Induces Cell Cycle Arrest via Downregulating the PI3K/AKT/<i>hTERT</i>Pathway in Lung Adenocarcinoma A549 Cells

PTENInhibits Cell Proliferation, Promotes Cell Apoptosis, and Induces Cell Cycle Arrest via Downregulating the PI3K/AKT/hTERTPathway in Lung Adenocarcinoma A549 Cells