Oncotarget · 2015 · 36 citations · 22 references
MedicineCancer BiologyOncologyMetastasisMolecular OncologySignal TransductionCancer Cell SignalingCancer ProgressionEpithelial-mesenchymal TransitionEpithelial-to-mesenchymal TransitionOncogenic Signaling PathwaysTumor InvasionCell Proliferation IndicesEpithelial-mesenchymal Transition In CancerEpithelial-mesenchymal Transition MarkersGallbladder CarcinomaMesenchymal TransitionOncogenic Signaling NetworksPhosphoinositide KinasesPi3k Signaling
// Shixian Lian 1, * , Yebo Shao 1, * , Houbao Liu 1, * , Junyi He 1, * , Weiqi Lu 1 , Yong Zhang 1 , Ying Jiang 1 , Jun Zhu 1 1 Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China * These authors have contributed equally to this work Correspondence to: Zhu J., e-mail: zhujun1024@126.com Keywords: 3-phosphoinositide-dependent protein kinase 1, JunB, invasion, migration, epithelial–mesenchymal transition Received: April 20, 2015 Accepted: July 23, 2015 Published: August 05, 2015 ABSTRACT The protein 3-phosphoinositide-dependent protein kinase 1 (PDK1) is upregulated in cancer. Here we showed that PDK1 stimulated cell proliferation, invasion and metastasis in gallbladder cancer (GBC), by inducing JunB and epithelial–mesenchymal transition. JunB levels were increased in GBC samples and positively correlated with PDK1 levels in tumors. High levels of JunB predicted poor overall survival in GBC patients. Thus, PDK1 functions as a tumor promoter in human GBC by upregulating JunB.
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A retroviral oncogene, akt, encoding a serine-threonine kinase containing an SH2-like region
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