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Activation of PTEN lipid phosphatase function in lung cancer

Activation of PTEN lipid phosphatase function in lung cancer content piece image

The low frequency of mutations in tumor suppressor PTEN undermines its role in lung cancer. Instead, PTEN expression/function is often reduced in lung tumors via several non-genomic mechanisms, resulting in hyper-activation of the oncogenic PI3K/AKT pathway. Kinase inhibitor (KI) therapy remains challenging due to off-target effects and generation of alternative signaling cascades following treatment. Direct activation of PTEN phosphatase activity represents a novel alternative therapeutic paradigm to attenuate PI3K/AKT signaling. Herein, we identify and characterize peptidomimetics that enhance PTEN lipid phosphatase activity and attenuate PI3K/AKT pathway signaling. Further, select compounds reduced proliferation, migration and induced cell cycle arrest in lung cancer cells, thereby acting as anticancer agents. We have also elucidated optimal PTEN-peptidomimetic interactions in silico. In summary, we have discovered novel small molecule compounds that directly induce PTEN function and antagonize PI3K/AKT pathway activity in lung cancer cells.