title: YAP overexpression promotes the epithelial-mesenchymal transition and chemoresistance in pancreatic cancer cells.
abstract: The expression of Yes-associated protein (YAP) has been reported to be dysregulated in pancreatic cancer. However, its contributions to tumor formation and progression remain to be elucidated. The present study demonstrated that YAP overexpression promoted the epithelial‑mesenchymal transition (EMT) in a manner associated with pancreatic cancer invasion in vitro. RNA interference‑mediated silencing of YAP attenuated cell invasion in vitro. Mechanistically, the present study demonstrated that YAP overexpression fosters pancreatic cancer progression by inducing the EMT in pancreatic cancer cells by activating the AKT cascade, which can counteract the effect of gemcitabine. These data suggested that the YAP acts synergistically to promote pancreatic cancer progression by hyperactivation of AKT signaling. The present study revealed YAP as a potential therapeutic target for pancreatic cancer and a biomarker for predicting gemcitabine treatment response.
authors.affiliation: Children's Hospital of Zhengzhou, Zhengzhou, Henan 450008, P.R. China.
authors.forename: Yanli
authors.initials: Y
authors.lastname: Yuan
authors.affiliation: Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
authors.forename: Deyu
authors.initials: D
authors.lastname: Li
authors.affiliation: Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
authors.forename: Haibo
authors.initials: H
authors.lastname: Li
authors.affiliation: Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
authors.forename: Liancai
authors.initials: L
authors.lastname: Wang
authors.affiliation: Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
authors.forename: Guangjin
authors.initials: G
authors.lastname: Tian
authors.affiliation: Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
authors.forename: Yadong
authors.initials: Y
authors.lastname: Dong
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism*; D045744:Cell Line, Tumor; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000494:pharmacology; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D006801:Humans; D009361:Neoplasm Invasiveness; D010190:Pancreatic Neoplasms / Q000201:enzymology / Q000473:pathology*; D010641:Phenotype; D010750:Phosphoproteins / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D014157:Transcription Factors; D015854:Up-Regulation / Q000187:drug effects; D000091102:YAP-Signaling Proteins; D000093542:Gemcitabine
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D010750:Phosphoproteins; D014157:Transcription Factors; D000091102:YAP-Signaling Proteins; C088374:YAP1 protein, human; D003841:Deoxycytidine; D051057:Proto-Oncogene Proteins c-akt; D000093542:Gemcitabine