Abstract
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.
Keywords: Astroglioma, Nifurtimox treatment, Temozolomide, in vivo, AKT-GSK3β, blood brain barrier.
Current Molecular Medicine
Title:Nifurtimox Hampered the Progression of Astroglioma In vivo Via Manipulating the AKT-GSK3β axis
Volume: 20 Issue: 9
Author(s): Qiuxia Zhang, Zhenshuai Chen, Wei Yuan, Yu-Qing Tang, Jiangli Zhu, Wentao Wu, Hongguang Ren, Hui Wang, Weiyi Zheng, Zhongjian Zhang*Eryan Kong*
Affiliation:
- Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang,China
- Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang,China
Keywords: Astroglioma, Nifurtimox treatment, Temozolomide, in vivo, AKT-GSK3β, blood brain barrier.
Abstract:
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:
Zhang Qiuxia , Chen Zhenshuai , Yuan Wei , Tang Yu-Qing, Zhu Jiangli , Wu Wentao , Ren Hongguang , Wang Hui , Zheng Weiyi , Zhang Zhongjian *, Kong Eryan *, 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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