Fig. 1.
Novel potential pharmacological approaches in neuroblastoma treatment. A MYCN-amplified neuroblastoma (NB) cells rely on fatty acid–dependent mitochondrial respiration. Inhibition of fatty acid oxidation (FAO) with inhibitor targeting carnitine palmitoyl-transferase 1a (CPT1) reduces tumor growth by inducing cell death. B Reactivation of fatty acid synthesis (FASN) in cancer cells is required for providing lipid building blocks for sustained cell proliferation. Inhibition of FASN by small molecules decreases cell proliferation and results in neural differentiation of NB cells. C Elongation of very-long-chain fatty acids–4 (ELOVL4) is required for the proper neural differentiation of NB cells (Rugolo et al. 2021). We hypothesize that NB cells treated with elovanoids (ELVs) may induce differentiation of NB cells. NB: neuroblastoma; ACSL4: acyl-CoA synthetase long-chain family member 4; TCA: tricarboxylic acid cycle; ETC: electron transport chain; ACACA: acetyl-CoA carboxylase alpha; FASN: fatty acid synthase; PUFA: polyunsaturated fatty acid; LC-PUFA: long-chain polyunsaturated fatty acid; VLC-PUFA: long-chain poly unsaturated fatty acid