@Article{096504018X15446984186056,
AUTHOR = {Zhenghua Fei,
 Zhenxiang Deng,
 Lingyang Zhou, Kejie Li, Xiaofang Xia, Raoying Xie},
TITLE = {PD-L1 Induces Epithelial–Mesenchymal Transition in Nasopharyngeal  Carcinoma Cells Through Activation of the PI3K/AKT Pathway},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {7},
PAGES = {801--807},
URL = {http://www.techscience.com/or/v27n7/48609},
ISSN = {1555-3906},
ABSTRACT = {Nasopharyngeal cancer (NPC) is a malignant epithelial carcinoma of the head and neck. Cancer therapy 
targeting programmed cell death protein-1 (PD-1) or programmed death ligand-1 (PD-L1) is revolutionary. 
However, the tumorigenic mechanism of PD-L1 is not yet clear in NPC. Here we demonstrated an oncogenic 
role of PD-L1 via activating PI3K/AKT in NPC cells. PD-L1 overexpression was frequently detected in NPC 
biopsies and cell lines by qRT-PCR. PD-L1 overexpression and knockdown demonstrated that PD-L1 promoted NPC cell invasion and metastasis in vitro and in vivo. Mechanistically, PD-L1 prominently activated the 
epithelial–mesenchymal transition (EMT) process in a PI3K/AKT-dependent manner. Taken together, we found 
that PD-L1 overexpression confers NPC cell malignancy and aggressiveness via activating the downstream 
PI3K/AKT signaling. Thus, these results provide a basis for diagnosis and treatment of NPC.},
DOI = {10.3727/096504018X15446984186056}
}