Amyloid β precursor protein silencing attenuates epithelial-mesenchymal transition of nasopharyngeal carcinoma cells via inhibition of the MAPK pathway

Advances in the treatment of nasopharyngeal carcinoma (NPC) have significantly improved the local control rate; however, distant metastasis remains a principal cause of mortality. Previous studies have demonstrated that the expression levels of amyloid beta precursor protein (APP) are increased in NPC. The present study aimed to investigate the association between APP and the development of NPC. In order to knockdown APP expression, an APP-small interfering RNA vector was synthesized and transfected into SUNE-1 cells. Cell Counting Kit-8 assay was performed to assess cell viability. The migratory and invasive abilities of SUNE-1 cells were examined by wound healing and Transwell assays, respectively. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to measure the mRNA and protein expression levels of APP, and additional factors involved in epithelial-mesenchymal transition (EMT) and in the mitogen-activated protein kinase (MAPK) signaling pathway. APP silencing significantly suppressed cell viability, migration and invasion. In addition, APP interference downregulated the expression levels of metastasis-associated 1, matrix metalloproteinase (MMP)-2 and MMP-9; however, knockdown of APP led to upregulation of tissue inhibitor of metalloproteinases 2 and inhibited EMT. The phosphorylation levels of p38, extracellular signal-regulated kinases 1/2 and c-Jun N-terminal kinases 1/2 were decreased following downregulation of APP. The present results suggested that APP knockdown may significantly inhibit the development of NPC by suppressing cell viability, migration and invasion, and by inhibiting the EMT process via downregulation of the MAPK signaling pathway. Therefore, APP may facilitate the development of a novel gene therapy for the treatment of NPC.