Nifurtimox hampered the progression of astroglioma in vivo via manipulating the AKT-GSK3βaxis

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. Our previous study demonstrated that nifurtimox could regulate the signaling axis of AKT-GSK3beta in vari ous 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. Our results exhibited that nifurtimox could competently hinder the development of astroglioma in 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. Persistently, the manipulation of the signaling axis of AKT-GSK3beta in astroglioma was found in line with earlier findings in neuroblastoma when treated with nifurtimox.