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The role of PHLPP in regulating cell migration in pancreatic cancer

Pancreatic cancer is the fourth leading cause of cancer in the United States. However, it has the worse prognosis of any malignancy with a 4% 5 year survival rate. Contributing factors include but not limited to late stage diagnosis due to vague symptoms and the degree of aggression associated with this type of cancer. Surgical resection is impossible in 50% of cases due to the advanced stage at the time of diagnosis. Pancreatic Ductal Adenocarcinoma (PDA) has a high rate of chemotherapy and radiation resistance increasing the need for innovative treatment modalities. Hyperactivation of PI3K/Akt pathways is commonly associated with many types of human cancers including pancreatic cancer. Recently, we have identified a novel protein phosphatase, PHLPP (PH domain Leucine repeat Protein Phosphatase) that dephosphorylates Akt and terminates Akt signaling directly. Our previous studies show that loss of PHLPP expression results in an increase in cell proliferation and a decrease in apoptosis. Here, we investigate the role of both PHLPP isoforms namely PHLPP1 and PHLPP2 in regulating pancreatic cancer cell migration and metastasis. Stable pancreatic cancer cell lines were generated using lentivirus‐based shRNAs to knockdown endogenous PHLPP expression. Alteration of Akt‐mediated signaling is analyzed in PHLPP knockdown cells. In addition, cell migration and invasion assays are performed to determine if loss of PHLPP expression promotes both tumorigenesis and metastasis in pancreatic cancer. The knowledge gained in these studies will provide a novel therapeutic avenue using PHLPP as a potential target.