Fig. 14From: Acetazolamide potentiates the anti-tumor potential of HDACi, MS-275, in neuroblastomaSchema depicting a potential mechanism of AZ and/or MS-275 treatments in NB cells. As illustrated, AZ, MS-275 and AZ + MS-275 treatments target survival pathways in NB cells. Alterations in cell cycle, and the HIF1-α/CAIX axis by AZ, MS-275 and AZ + MS-275 could affect the NB cell transit amplifying cell population, and its proliferation and survival. Importantly, these treatments could additionally target the CSC in NB by perturbation of self-renewal potential, stem cell state and the SP phenotype. The pan-inhibition of these pathways and critical components would ultimately decrease the tumorigenic potential of NB cells and lead to elimination of the tumor cellsBack to article page