Xu Yice, Tao Zezhang, Jiang Yang, Liu Tao, Xiang Yinzhou
Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University Wuhan, Hubei, P. R. China.
Int J Clin Exp Pathol. 2019 Jan 1;12(1):356-364. eCollection 2019.
Nasopharyngeal carcinoma (NPC) is a respiratory malignant epithelial carcinoma. Research has indicated that bactericidal/permeability-increasing fold-containing protein B1 (BPIFB1), mostly secreted by nasopharyngeal epithelia, is dysregulated in patients with NPC. This study aimed to explore the effects of BPIFB1 inviability, proliferation, apoptosis and its molecular mechanism. To confirm the effects of BPIFB1 on NPC cells, BPIFB1 was overexpressed or silenced in NPC-KT cells after being transfected with BPIFB1 or siBPIFB1 plasmids. The results showed that BPIFB1 overexpression could induce apoptosis and DNA damage in NPC-KT cells, and silenced BPIFB1 had the opposite effects. BPIFB1 overexpression can inhibit the cell cycle by being arrested at the G0/G1 phase and by regulating the MEK/ERK signaling pathway. MEK inhibitor U0126 was used to confirm the effects of BPIFB1 on the MEK/ERK pathway, and U0126 can inverse the effects of siBPIFB1. Additionally, BPIFB1 can enhance the anti-proliferative effect of chemotherapy drugs on NPC-KT cells. All the results indicated that BPIFB1 could be a potential target for the treatment of NPC.
鼻咽癌（NPC）是一种呼吸道恶性上皮癌。研究表明，主要由鼻咽上皮分泌的含杀菌/通透性增加折叠蛋白B1（BPIFB1）在鼻咽癌患者中表达失调。本研究旨在探讨BPIFB1在细胞活力、增殖、凋亡方面的作用及其分子机制。为了证实BPIFB1对鼻咽癌细胞的作用，用BPIFB1或siBPIFB1质粒转染NPC-KT细胞后，使BPIFB1过表达或沉默。结果表明，BPIFB1过表达可诱导NPC-KT细胞凋亡和DNA损伤，而沉默BPIFB1则产生相反的效果。BPIFB1过表达可通过使细胞周期停滞在G0/G1期并调节MEK/ERK信号通路来抑制细胞周期。使用MEK抑制剂U0126来证实BPIFB1对MEK/ERK通路的作用，U0126可逆转siBPIFB1 的作用。此外，BPIFB1可增强化疗药物对NPC-KT细胞的抗增殖作用。所有结果表明，BPIFB1可能是鼻咽癌治疗的一个潜在靶点。
