Title:Nifurtimox Hampered the Progression of Astroglioma <i>In vivo</i> 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* and Eryan Kong*
Affiliation:Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang, Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang, Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang, School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, Department of Ophthalmology, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang 453000, Tianjin Ocelean Pharma, Tianjin, Tianjin Ocelean Pharma, Tianjin, Henan Key Laboratory of Immunology and Targeted Therapy, Xinxiang, School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang, Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang
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.
