Open Access

ARTICLE

PD-L1 Induces Epithelial–Mesenchymal Transition in Nasopharyngeal Carcinoma Cells Through Activation of the PI3K/AKT Pathway

Zhenghua Fei^*1, Zhenxiang Deng^†1, Lingyang Zhou^‡, Kejie Li^*, Xiaofang Xia^*, Raoying Xie^*

* Department of Radiation and Medical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Zhejiang, P.R. China
† Department of Radiation Oncology, Xiang’an Hospital of Xiamen University, Fujian, P.R. China
‡ Department of General Surgery, Yongjia County Traditional Chinese Medicine Hospital, Zhejiang, P.R. China

Oncology Research 2019, 27(7), 801-807. https://doi.org/10.3727/096504018X15446984186056

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.

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