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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 in
vitro, and inhibited tumor growth in vivo. 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.