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去铁酮增强替莫唑胺对胶质瘤细胞的细胞毒性。

Deferiprone Enhances Temozolomide Cytotoxicity in Glioma Cells.

作者信息

Alexiou George A, Gerogianni Paraskevi, Vartholomatos Evrysthenis, Kyritsis Athanasios P

机构信息

a Neurosurgical Institute, University of Ioannina , Ioannina , Greece.

出版信息

Cancer Invest. 2016 Nov 25;34(10):489-495. doi: 10.1080/07357907.2016.1233424. Epub 2016 Oct 21.

DOI:10.1080/07357907.2016.1233424
PMID:27768402
Abstract

Glioblastoma is the most malignant primary brain tumor with a median survival of 15 months. Temozolomide (TMZ) is the standard of care for these patients. Iron chelators have been shown to have anti-tumor activity; however, deferiprone (DFP), an orally administered iron chelator, has not been previously evaluated in gliomas. In the present study, we found that combination treatment in glioma cells with TMZ and DFP significantly reduced cell viability, produced cell cycle arrest at G2/M phase, and enhanced apoptosis. TMZ and DFP might be a potent new combination treatment for glioblastoma.

摘要

胶质母细胞瘤是最恶性的原发性脑肿瘤,中位生存期为15个月。替莫唑胺(TMZ)是这些患者的标准治疗药物。铁螯合剂已显示出具有抗肿瘤活性;然而,去铁酮(DFP),一种口服铁螯合剂,此前尚未在胶质瘤中进行评估。在本研究中,我们发现胶质瘤细胞中TMZ与DFP联合治疗显著降低细胞活力,使细胞周期停滞在G2/M期,并增强细胞凋亡。TMZ和DFP可能是胶质母细胞瘤一种有效的新联合治疗方法。

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1
Deferiprone Enhances Temozolomide Cytotoxicity in Glioma Cells.去铁酮增强替莫唑胺对胶质瘤细胞的细胞毒性。
Cancer Invest. 2016 Nov 25;34(10):489-495. doi: 10.1080/07357907.2016.1233424. Epub 2016 Oct 21.
2
NVP-BEZ235, a novel dual PI3K-mTOR inhibitor displays anti-glioma activity and reduces chemoresistance to temozolomide in human glioma cells.NVP-BEZ235,一种新型的双重 PI3K-mTOR 抑制剂,在人神经胶质瘤细胞中显示出抗神经胶质瘤活性,并降低替莫唑胺的化疗耐药性。
Cancer Lett. 2015 Oct 10;367(1):58-68. doi: 10.1016/j.canlet.2015.07.007. Epub 2015 Jul 15.
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Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells.自噬在替莫唑胺诱导恶性胶质瘤细胞毒性中的作用。
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KCa3.1 channel inhibition sensitizes malignant gliomas to temozolomide treatment.KCa3.1通道抑制可使恶性胶质瘤对替莫唑胺治疗敏感。
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Delayed repletion of O6-methylguanine-DNA methyltransferase resulting in failure to protect the human glioblastoma cell line SF767 from temozolomide-induced cytotoxicity.O6-甲基鸟嘌呤-DNA甲基转移酶的延迟补充导致无法保护人胶质母细胞瘤细胞系SF767免受替莫唑胺诱导的细胞毒性。
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Inhibition of c-Jun N-terminal kinase enhances temozolomide-induced cytotoxicity in human glioma cells.抑制 c-Jun N-末端激酶增强替莫唑胺诱导的人胶质瘤细胞毒性。
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p53 effects both the duration of G2/M arrest and the fate of temozolomide-treated human glioblastoma cells.p53对G2/M期阻滞的持续时间以及替莫唑胺治疗的人胶质母细胞瘤细胞的命运均有影响。
Cancer Res. 2001 Mar 1;61(5):1957-63.
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TMZ-induced PrPc/par-4 interaction promotes the survival of human glioma cells.TMZ 诱导的 PrPc/par-4 相互作用促进人神经胶质瘤细胞的存活。
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Resveratrol abrogates the temozolomide-induced G2 arrest leading to mitotic catastrophe and reinforces the temozolomide-induced senescence in glioma cells.白藜芦醇废除了替莫唑胺诱导的 G2 期阻滞,导致有丝分裂灾难,并增强了替莫唑胺诱导的神经胶质瘤细胞衰老。
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Guanosine promotes cytotoxicity via adenosine receptors and induces apoptosis in temozolomide-treated A172 glioma cells.鸟苷通过腺苷受体促进细胞毒性,并诱导替莫唑胺处理的 A172 神经胶质瘤细胞凋亡。
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