Overexpression of BPIFB1 promotes apoptosis and inhibits proliferation via the MEK/ERK signal pathway in nasopharyngeal carcinoma.

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.