Nrf-2 and HO-1 Expression in Medulloblastoma: A Clinicopathological Analysis

Abstract

Medulloblastoma (MB) is one of the most common malignant tumors with poor survival in children. Nuclear factor erythroid 2-related factor2 (Nrf-2) and heme oxygenase-1 (HO-1) have been considered to play major roles in the pathogenesis of many tumors. There is no report about clinicopathological significance of Nrf-2 and HO-1 expression in medulloblastoma. In the present study, to explore the expression and potential function of Nrf-2 and HO-1 in MBs, immunohistochemistry was used to examine the Nrf-2 and HO-1 expression in 41 MBs and 27 control tissues adjacent to the tumor. The results showed that in the cases of MB, the positive expression rates of Nrf-2 and HO-1 (82.9% and 78.0%) were significantly increased compared with that (37.0% and 29.6%) in peritumoral control brain tissues. The difference was statistically significant (P < 0.001). A positive correlation between the expression of Nrf-2 and HO-1 in MB (r = 0.542, P < 0.05) was observed. However, there was no definite correlation among the expression of Nrf-2 and HO-1 and the clinical pathological features (P > 0.05). The abnormal expression of Nrf-2 and HO-1 in MB suggest that the Nrf-2/HO-1 pathway plays an important role in the formation and development of MB and may be a potential therapeutic target for MB.

Pathological implications of metabolic reprogramming and its therapeutic potential in medulloblastoma

“…In contrast to the significant amount of literature linking NRF2 with adult GBM, the current knowledge about its clinicopathological significance in MB is still poor. In a work from Tang et al, 2017 it has been demonstrated that NRF2 expression is enhanced in MB samples (n = 41) when compared to peritumoral control brain tissues (n = 27). Moreover, it was previously shown that pharmacological targeting of NRF2 with two NRF2-inducers (nifurtimox and tetrathiomolybdate) results in a synergic ROS-dependent antitumor response towards MB in vitro ( Koto et al, 2011 ).…”