Open AccessYAP overexpression promotes the epithelial-mesenchymal transition and chemoresistance in pancreatic cancer cells
Author(s) -
Yanli Yuan,
Deyu Li,
Haibo Li,
Liancai Wang,
Guangjin Tian,
Yadong Dong
Publication year - 2015
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2015.4550
Subject(s) - pancreatic cancer , epithelial–mesenchymal transition , oncogene , cancer research , gene silencing , gemcitabine , protein kinase b , cancer , cell cycle , tumor progression , molecular medicine , biology , cancer cell , signal transduction , metastasis , medicine , microbiology and biotechnology , gene , biochemistry
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.
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