Loss of RAB1B promotes triple-negative breast cancer metastasis by activating TGF-β/SMAD signaling - Jiang, Hong-Lin; Sun, He-Fen; Gao, Shui-Ping; Li, Liang-Dong; Hu, Xin; Wu, Jiong; Jin, Wei (Oncotarget, 2015)
Keywords: Animals; Biomarkers, Tumor - genetics; Carcinoma, Ductal, Breast - genetics; Carcinoma, Ductal, Breast - mortality; Carcinoma, Ductal, Breast - pathology; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Down-Regulation; Enzyme Activation - genetics; Epithelial-Mesenchymal Transition - genetics; Female; Gene Expression Regulation, Neoplastic; HEK293 Cells; Heterografts; Humans; Lung Neoplasms - secondary; Mice; Mice, Inbred BALB C; Mice, Nude; Middle Aged; Neoplasm Transplantation; Prognosis; rab1 GTP-Binding Proteins - genetics; Receptors, Transforming Growth Factor beta - metabolism; Research Paper; RNA Interference; RNA, Small Interfering; Signal Transduction - genetics; Smad3 Protein - metabolism; Tissue Array Analysis; Transforming Growth Factor beta - metabolism; Triple Negative Breast Neoplasms - genetics; Triple Negative Breast Neoplasms - mortality; Triple Negative Breast Neoplasms - pathology; Ubiquitin - metabolism; TGF-β/SMAD signaling; triple-negative; RAB1B; metastatic breast cancer