As one of the main pathological changes of Parkinson's disease (PD), axonal degeneration was thought to be a passive process that is secondary to the apoptosis of dopaminergic neurons and, therefore, it has been overlooked for some time. Recent research, however, has indicated that axonal injury is the first location of damage in dopaminergic neurons in PD, and that the degree of injury in axonal degeneration is higher than in neural death.
MSP58, a novel oncogene, shows transforming activity in mouse embryonic fibroblasts. However, the oncogenic role of MSP58 in tumor cells has not been fully characterized. To extend understanding of how this protein operates in tumorigenesis, we aimed to identify the effect of MSP58 on neuroblastoma cell proliferation. Here, we found that MSP58 was highly expressed in neuroblastoma tumor samples and cell lines. We found that the majority of MSP58 protein can be detected in the nucleus as reported in other cells. Moreover, MSP58-targeted shRNA lentivirus attenuated neuroblastoma cell proliferation. Knockdown of MSP58 resulted in S-phase cell accumulation, which was accompanied by changes in cell cycle-related molecules. These results indicate that MSP58 plays an oncogenic role in the proliferation of neuroblastoma cells and could be a novel target for the treatment of neuroblastoma.
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