Journal
MOLECULAR MEDICINE REPORTS
Volume 11, Issue 2, Pages 924-930Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2799
Keywords
nasopharyngeal carcinoma; ephrin type-A receptor 2; drug resistance; paclitaxel; phosphoinositide 3-kinase/Akt
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Funding
- National Natural Science Foundation of China [81202128, 81272974, 81372426]
- Research Fund for the Doctoral Program of Higher Education of China [20120162120049, 20100162110036]
- Freedom Explore Program of Central South University [2012QNZT099]
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Ephrin type-A receptor 2 (EphA2) is a receptor tyrosine kinase that is associated with cancer cell metastasis. There has been little investigation into its impact on the regulation of sensitivity to paclitaxel in nasopharyngeal carcinoma (NPC). In the present study, upregulation of EphA2 expression enhanced the survival of NPC 5-8F cells, compared with control cells exposed to the same concentrations of paclitaxel. Flow cytometry and western blot analysis demonstrated that over-expression of EphA2 decreased NPC cancer cell sensitivity to paclitaxel by regulating paclitaxel-mediated cell cycle progression but not apoptosis in vitro. This was accompanied by alterations in the expression of cyclin-dependent kinase inhibitors, p21 and p2'7, and of inactive phosphorylated-retinoblastoma protein. Furthermore, paclitaxel stimulation and EphA2 over-expression resulted in activation of the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway in NPC cells. Inhibition of the PI3K/Akt signalling pathway restored sensitivity to paclitaxel in 5-8F cells over-expressing EphA2, which indicated that the PI3K/Akt pathway is involved in EphA2-mediated paclitaxel sensitivity. The current study demonstrated that EphA2 mediates sensitivity to paclitaxel via the regulation of the PI3K/Akt signalling pathway in NPC.
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