DEK promoted EMT and angiogenesis through regulating PI3K/AKT/mTOR pathway in triple-negative breast cancer

// Yang Yang 1, * , Meihua Gao 2, * , Zhenhua Lin 1 , Liyan Chen 3 , Yu Jin 4 , Guang Zhu 1 , Yixuan Wang 1 and Tiefeng Jin 1 1 Department of Pathology, Cancer Research Center, Yanbian University Medical College, Yanji 133002, China 2 Department of Internal Medicine, Yanbian University Hospital, Yanji 133000, China 3 Department of Biochemistry and Molecular Biology, Yanbian University Medical College, Yanji 133002, China 4 Department of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji 133002, China * These authors have contributed equally to this work Correspondence to: Tiefeng Jin, email: jintf@ybu.edu.cn Keywords: DEK, prognosis, angiogenesis, metastasis, triple-negative breast cancer Received: May 24, 2017     Accepted: September 21, 2017     Published: October 17, 2017 ABSTRACT Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer associated with poor prognosis. As an oncogene, DEK involves in regulation of various cellular metabolisms and plays an important role in tumor growth and progression. Increasing evidences suggested that abnormal expression of DEK is closely related to multiple malignant tumors. However, the possible involvement of DEK in epithelial to mesenchymal transition (EMT) and angiogenesis in TNBC remains unclear. In the present study, we revealed that the over-expression of DEK was significantly correlated with clinical stage, differentiation, and lymph node (LN) metastasis of TNBC and indicated poor overall survival of TNBC patients. Moreover, we demonstrated that DEK depletion could significantly reduce cell proliferation, migration, invasion and angiogenesis in vitro . We also found that DEK promoted cancer cell angiogenesis and metastasis by activating the PI3K/AKT/mTOR pathway. Furthermore, we revealed the inhibitory effect of DEK depletion on tumor growth and progression in a xenograft tumor model in mice. These data indicated that DEK promotes TNBC cell proliferation, angiogenesis, and metastasis via PI3K/AKT/mTOR signaling pathway, and therefore, it might be a potential target in TNBC therapy.