Icariside II targets in vitro MAPK and PI3K/Akt signaling in human nasopharyngeal carcinoma cells to induce apoptotic death and suppress proliferation

Abstract

Abstract Background Icariside II is a derivative of Herba Epimedii, which is a traditional Chinese medicine. While prior reports have demonstrated that this flavonoid exerts a diverse array of antitumor activities when used to treat different human tumor cells, its impact on nasopharyngeal carcinoma (NPC) cells remains to be rigorously investigated. Methods In this study, MTT assays and flow cytometry were used to examine the impact of icariside II treatment on the proliferative and apoptotic activity of NPC cells in vitro. In addition, changes in MAPK and PI3K/Akt pathway activation were examined via qPCR and Western immunoblotting. Results Together, these analyses suggested that icariside II was able to markedly suppress NPC proliferation in a dose- and time-dependent fashion. Mechanistically, exposure to this flavonoid promoted the apoptotic death of the CNE1 and CNE2 cell lines through the simultaneous downregulation of Bcl-2 and the upregulation of Bax. In addition, icariside II suppress ERK1/2 and Akt phosphorylation while enhancing p38 phosphorylation. Conclusions As such, icariside II is capable of inhibiting NPC cell proliferation and inducing apoptotic death at least in part by modulating MAPK and PI3K/Akt signaling.