β-arrestin1 promotes epithelial-mesenchymal transition via modulating GSK-3β/β-catenin pathway in prostate cancer cells

Recently, β-arrestin1 was indicated as a tumor promoter in prostate cancer, but its exact role in cancer metastasis still have not been well clarified. Here, our data revealed that β-arrestin1 could promote the migration and invasion of prostate cancer cells via initiating epithelial-mesenchymal transition (EMT). Mechanically, β-arrestin1 could increase the transcriptional activity and expression of β-catenin, together with Akt activity, whereas decrease the activities of GSK-3β and PP2A. In addition, β-arrestin1 could function as a scaffold protein in modulating the interactions between PP2A, Akt, GSK-3β and β-catenin. These results reveal a novel mechanism of β-arrestin1 in modulating EMT and GSK-3β/β-catenin signaling in prostate cancer, thereby suggest that assessment of β-arrestin1 may provide a potential therapeutic target for prostate cancer.