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首页> 外文期刊>Journal of Cellular Physiology >Sorafenib/Regorafenib and Lapatinib Interact to kill CNS Tumor Cells
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Sorafenib/Regorafenib and Lapatinib Interact to kill CNS Tumor Cells

机译：索拉非尼/ Regorafenib和拉帕替尼进行交互杀了中枢神经系统肿瘤细胞

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The present studies were to determine whether the multi-kinase inhibitor sorafenib or its derivative regorafenib interacted with the ERBB1/ERBB2 inhibitor lapatinib to kill CNS tumor cells. In multiple CNS tumor cell types sorafenib and lapatinib interacted in a greater than additive fashion to cause tumor cell death. Tumor cells lacking PTEN, and anoikis or lapatinib resistant cells were as sensitive to the drug combination as cells expressing PTEN or parental cells, respectively. Similar data were obtained using regorafenib. Treatment of brain cancer cells with [sorafenib+lapatinib] enhanced radiation toxicity. The drug combination increased the numbers of LC3-GFP vesicles; this correlated with a reduction in endogenous LC3II, and p62 and LAMP2 degradation. Knock down of Beclin1 or ATG5 significantly suppressed drug combination lethality. Expression of c-FLIP-s, BCL-XL, or dominant negative caspase 9 reduced drug combination toxicity; knock down of FADD or CD95 was protective. Expression of both activated AKT and activated MEK1 or activated mTOR was required to strongly suppress drug combination lethality. As both lapatinib and sorafenib are FDA approved agents, our data argue for further determination as to whether lapatinib and sorafenib is a useful glioblastoma therapy. J. Cell. Physiol. 229: 131-139, 2014. (c) 2014 Wiley Periodicals, Inc.
机译：目前的研究确定multi-kinase抑制剂索拉非尼或其导数regorafenib与互动ERBB1 / ERBB2抑制剂拉帕替尼杀死中枢神经系统肿瘤细胞。拉帕替尼在大于互动添加剂的方式导致肿瘤细胞死亡。细胞缺乏PTEN和女性或拉帕替尼耐药细胞对药物敏感结合细胞PTEN表达或父母细胞,分别。使用regorafenib。细胞[索拉非尼+拉帕替尼]增强辐射毒性。增加的数量LC3-GFP囊泡;与减少内生LC3II,和p62 LAMP2退化。Beclin1或ATG5显著抑制药物组合杀伤力。BCL-XL或主导-半胱天冬酶9减少毒性药物组合;CD95防护。AKT激活MEK1或激活mTOR要求强烈抑制药物组合杀伤力。FDA批准的代理,我们的数据进一步主张拉帕替尼是否和决心索拉非尼是一种有用的胶质母细胞瘤的治疗。细胞。期刊、公司。

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