TY - JOUR AB - Glioblastoma multiforme (GBM) is the most common and severe form of primary tumor in the central nervous system of adults which has poor prognosis and limited therapeutic options. Epidermal growth factor receptor (EGFR) inhibitor, such as gefitinib (brand name Iressa, ZD1839), has been approved as a targeted medicine for several types of tumor including glioblastoma multiforme. However, gefitinib exerted very limited effects on some glioblastoma multiforme patients after a period of treatment due to intrinsic and acquired drug resistance. β-Elemene, a natural plant drug extracted from Curcuma wenyujin, has shown promising anticancer effects against a broad spectrum of tumors. In the present study, we found that β-elemene could enhance the chemosensitivity of glioblastoma multiforme cells to gefitinib. The combination medication of β-elemene and gefitinib not only inhibited the survival and proliferation of glioblastoma multiforme cells via inhibition of EGFR signaling pathway but also induced more distinct apoptosis and autophagy in the glioblastoma multiforme cells than the gefitinib monotherapy. These results showed that β-elemene might be one potential adjuvant to enhance the effect of EGFR inhibitor and reduce the resistance of gefitinib in glioblastoma multiforme. AD - The First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116011, P.R. China AU - Mu,Lin AU - Wang,Tianjiao AU - Chen,Yanwei AU - Tang,Xinqiang AU - Yuan,Yuhui AU - Zhao,Yongshun DA - 2016/10/01 DO - 10.3892/ijo.2016.3626 EP - 1436 IS - 4 JO - Int J Oncol KW - glioblastoma multiforme β-elemene gefitinib epidermal growth factor receptor pathway chemosensitivity PY - 2016 SN - 1019-6439 1791-2423 SP - 1427 ST - β-Elemene enhances the efficacy of gefitinib on glioblastoma multiforme cells through the inhibition of the EGFR signaling pathway T2 - International Journal of Oncology TI - β-Elemene enhances the efficacy of gefitinib on glioblastoma multiforme cells through the inhibition of the EGFR signaling pathway UR - https://doi.org/10.3892/ijo.2016.3626 VL - 49 ER -