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Marsdenia tenacissima extract restored gefitinib sensitivity in resistant non-small cell lung cancer cells
Han, Shu-Yan1; Zhao, Ming-Bo2; Zhuang, Gui-Bao1; Li, Ping-Ping1
关键词Marsdenia tenacissima extract Gefitinib resistance NSCLC T790M K-ras mutations
刊名LUNG CANCER
2012
DOI10.1016/j.lungcan.2011.06.001
75期:1页:30-37
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Respiratory System
研究领域[WOS]Oncology ; Respiratory System
关键词[WOS]GROWTH-FACTOR-RECEPTOR ; TYROSINE KINASE INHIBITORS ; MEDIATED MULTIDRUG-RESISTANCE ; MET AMPLIFICATION ; ACQUIRED-RESISTANCE ; T790M MUTATION ; EGFR T790M ; POLYOXYPREGNANE GLYCOSIDES ; 1ST-LINE GEFITINIB ; THERAPY
英文摘要

Most non-small cell lung cancer (NSCLC) patients responding to gefitinib harbor activating mutations in the epidermal growth factor receptor (EGFR). However, the responsive cases eventually develop the resistance to gefitinib. Besides, K-ras mutations were identified as the primary resistance to gefitinib. We investigated whether Marsdenia tenacissima extract (MTE, trade name: Xiao-Ai-Ping injection) combined with gefitinib could overcome the resistance of NSCLC cells to gefitinib. NSCLC cell lines with different sensitivities to gefitinib were studied. Cell growth and apoptosis were evaluated by MTT assay and flow cytometry, respectively. The EGFR-related signaling molecule phosphorylation was assessed by Western blotting. We found that MTE inhibited cell growth in gefitinib-sensitive and -resistant cells. In gefitinib-resistant cells, the MTE -> MTE + gefitinib (M -> M + G) treatment was most potent over the concurrent administration of MTE and gefitinib (M + G) or gefitinib -> gefitinib + MTE (G -> G + M) treatment in cell growth inhibition and apoptosis induction. The M -> M + G treatment significantly reduced the phosphorylation of EGFR downstream signaling molecules PI3K/Akt/mTOR and ERK, on which MTE and gefitinib alone had no obvious effects on the resistant cells. The M -> M + G treatment attenuated c-Met phosphorylation in H460 and H1975 as well. Thus, we found that the M -> M + G treatment improved the sensitivity of resistant NSCLC cells carrying 1790 M or K-ras mutations to gefitinib, suggesting that the M -> M + G treatment may be a promising therapeutic strategy to overcome gefitinib resistance in NSCLC. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

语种英语
WOS记录号WOS:000299450600005
项目编号20090450009 ; 7112027
资助机构China Postdoctoral Science Foundation ; Beijing Natural Science Foundation
引用统计
被引频次:36[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/58608
专题北京大学药学院
北京大学药学院_天然药物学系
北京大学临床肿瘤学院_中西医结合科暨老年肿瘤科
作者单位1.Peking Univ, Dept Integrat Chinese & Western Med, Sch Oncol,Beijing Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100142, Peoples R China
2.Peking Univ, Hlth Sci Ctr, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Han, Shu-Yan,Zhao, Ming-Bo,Zhuang, Gui-Bao,et al. Marsdenia tenacissima extract restored gefitinib sensitivity in resistant non-small cell lung cancer cells[J]. LUNG CANCER,2012,75(1):30-37.
APA Han, Shu-Yan,Zhao, Ming-Bo,Zhuang, Gui-Bao,&Li, Ping-Ping.(2012).Marsdenia tenacissima extract restored gefitinib sensitivity in resistant non-small cell lung cancer cells.LUNG CANCER,75(1),30-37.
MLA Han, Shu-Yan,et al."Marsdenia tenacissima extract restored gefitinib sensitivity in resistant non-small cell lung cancer cells".LUNG CANCER 75.1(2012):30-37.
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