摘要
背景:星形胶质瘤是脑肿瘤的一种主要形式,由于肿瘤病理学的复杂性以及对化学疗法和放射疗法的不良反应,几十年来一直很难处理。 方法:我们先前的研究表明,尼富替莫可调节AKT-GSK3β在各种类型的肿瘤(包括星形胶质瘤U251细胞)中的信号传导轴。有趣的是,较早的案例研究表明硝呋替莫可能渗透血脑屏障并阻止脑神经母细胞瘤。这些观察结果共同鼓励我们探讨尼富替莫是否会在体内阻碍星形胶质瘤的生长。 结果:我们的结果表明,与替莫唑胺相比,尼替莫司能有效地抑制小鼠脑星形胶质瘤的发展,替莫唑胺是治疗脑肿瘤的第一线药物。同时,与替莫唑胺相比,硝呋替莫治疗后存活率和体重显着上调。这些发现提供了尼呋替莫作为体内治疗星形胶质瘤的更好的替代药物。 结论:持久地,星形胶质瘤中发现了AKT-GSK3β信号轴的操纵与尼古丁酮治疗时神经母细胞瘤的早期发现一致。
关键词: 星形胶质瘤,尼呋替莫治疗,替莫唑胺,体内,AKT-GSK3β,血脑屏障。
Current Molecular Medicine
Title:Nifurtimox Hampered the Progression of Astroglioma In vivo Via Manipulating the AKT-GSK3β axis
Volume: 20 Issue: 9
关键词: 星形胶质瘤,尼呋替莫治疗,替莫唑胺,体内,AKT-GSK3β,血脑屏障。
摘要:
Background: Astroglioma, one major form of brain tumors, has remained principally tough to handle for decades, due to the complexity of tumor pathology and the poor response to chemo- and radio-therapies.
Methods: Our previous study demonstrated that nifurtimox could regulate the signaling axis of AKT-GSK3β in various tumor types including the astroglioma U251 cells. Intriguingly, earlier case studies suggested that nifurtimox could possibly permeate the blood brain barrier and arrest neuroblastoma in the brain. These observations jointly encouraged us to explore whether nifurtimox would hinder the growth of astroglioma in vivo.
Results: Our results exhibited that nifurtimox could competently hinder the development of astroglioma in the mouse brain as compared to temozolomide, the first line of drug for brain tumors. Meanwhile the surviving rate, as well as the body-weight was dramatically upregulated upon nifurtimox treatment, as compared to that of temozolomide. These findings offered nifurtimox as a better alternative drug in treating astroglioma in vivo.
Conclusion: Persistently, the manipulation of the signaling axis of AKT-GSK3β in astroglioma was found in line with earlier findings in neuroblastoma when treated with nifurtimox.
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Cite this article as:
Nifurtimox Hampered the Progression of Astroglioma In vivo Via Manipulating the AKT-GSK3β axis, Current Molecular Medicine 2020; 20 (9) . https://dx.doi.org/10.2174/1566524020666200409124258
DOI https://dx.doi.org/10.2174/1566524020666200409124258 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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