Assessment of anti-cancer activity of cyclovirobuxine D in nasopharyngeal carcinoma cells: Involvement of KIF23-mediated Akt/mTOR pathway

Cyclovirobuxine D (CVB-D) is a phytochemical ingredient that has potential antitumor effects in several types of Cancer. However, its role and action mechanism in nasopharyngeal carcinoma (NPC) are still unclear. The present study found that CVB-D inhibited the viability of NPC cells, as well as induced NPC cell Apoptosis. Kinesin family member 23 (KIF23) expression was inhibited by CVB-D treatment, and KIF23 knockdown exhibited viability-inhibitory and pro-apoptotic effects on NPC cells. Next, we demonstrated that overexpression of KIF23 prevented the inhibitory effect of CVB-D on cell viability, as well as its inductive effect on cell Apoptosis. CVB-D treatment or KIF23 knockdown inhibited the Akt/mTOR pathway activation in NPC cells, with decreased expression levels of p-Akt and p-mTOR. Overexpression of KIF23 blocked the inhibitory effect of CVB-D on Akt/mTOR pathway activation. Additionally, Akt knockdown resisted KIF23-mediated antitumor effect of CVB-D. Our results indicated that CVB-D exerted viability-inhibitory and pro-apoptotic effects on NPC cells with the involvement of the KIF23/Akt/mTOR pathway. We provided experimental evidence for the antitumor potential and therapeutic implication of CVB-D in NPC.

Akt/mTOR pathway; Apoptosis; KIF23; Nasopharyngeal carcinoma; Viability.