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Dedicator of cytokinesis 1 (DOCK1) is an important regulator of tumorigenesis in various human cancers, yet its role in prostate cancer remains unknown. In this study, we examined the role of DOCK1 as a potential biomarker in tumorigenesis and its regulation mechanism as well as clinical values in prostate cancer. We found DOCK1 knockout inhibited cell proliferation, viability, and migration, and promoted cell apoptosis of prostate cancer cells <i>in vitro,</i> and inhibited tumor growth <i>in vivo</i>. Mechanistically, knockout of DOCK1 hampered epithelial-mesenchymal transition (EMT) characterized by the decrease of Snail, N-cadherin, and MMP9 expression and the increase in E-Cadherin by enhancing the phosphorylation of AKT. In addition, INPP4B、HPGD、IGFBP5 and IL1R2 genes were upregulated, and PRKACB、TMSB4X and CCND1 downregulated in DOCK1 knockout cells. Moreover, immunohistochemistry analysis in prostate cancer tissue array showed that DOCK1 upregulation was related to unfavorable prognosis in prostate cancer patients. DOCK1 acts as an oncogenic factor by regulating EMT via AKT signaling in prostate cancer. DOCK1 may be potentially used as a novel therapeutic target for prostate cancer treatment.