ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism - Liu, Mingyang; Yang, Jingxuan; Zhang, Yuqing; Zhou, Zhijun; Cui, Xiaobo; Zhang, Liyang; Fung, Kar-Ming; Zheng, Wei; Allard, Felicia D.; Yee, Eric U.; Ding, Kai; Wu, Huanwen; et al. (Clinical cancer research, 2018)
Keywords: Animals; Biotechnology; Cancer; Cation Transport Proteins - metabolism; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Claudin-1 - genetics; Deactivation; Disease Models, Animal; Disease Progression; Epithelial-Mesenchymal Transition; Experimental design; Functional analysis; Gene expression; Gene Expression Regulation, Neoplastic; Genetic engineering; Heterografts; Humans; Immunohistochemistry; Inactivation; Invasiveness; Metastases; Metastasis; Mice; Models, Biological; Neoplasia; Neoplasm Staging; Pancreatic cancer; Pancreatic Neoplasms - genetics; Pancreatic Neoplasms - metabolism; Pancreatic Neoplasms - pathology; Paxillin; Phosphorylation; Signal Transduction; Therapeutic applications; Transcription; Transcription, Genetic; Tumor cell lines; Tumors; Xenografts; Xenotransplantation; Zinc Finger E-box-Binding Homeobox 1 - metabolism; Zonula occludens-1 protein; Zonula Occludens-1 Protein - genetics