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
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