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. 2014 Oct 29;11(2):924–930. doi: 10.3892/mmr.2014.2799

Figure 5.

Figure 5

EphA2 mediated paclitaxel sensitivity in NPC 5–8 cells via modulation of the PI3K/Akt signalling pathway. (A) PI3K/Akt signalling pathway inhibitor, LY294002, reverses paclitaxel resistance caused by EphA2 over-expression. (B) Effect of LY294002 on the cell-cycle distribution in EphA2 over-expressing NPC cells pre-treated with paclitaxel. (C) Effect of LY294002 on the apoptotic rate in NPC cells over-expressing EphA2, pretreated with paclitaxel. (D) LY294002 restores the changes in expression of cyclin-dependent kinase inhibitors, p21Cip1 and p27Kip1, caused by EphA2 over-expression. *P<0.05. EphA2, ephrin type-A receptor 2; NPC, nasopharyngeal carcinoma; PI3K, phosphoinositide 3-kinase; p-Akt, phsophorylated Akt; Rb, retinoblastoma protein; p-Rb, phosphorylated Rb.