Division of Hematology-Oncology, Department of Medicine, Abramson Cancer Center, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Cell. 2012 Mar 30;149(1):22-35. doi: 10.1016/j.cell.2012.03.003.
The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to therapeutic opportunities. MYC's activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.
MYC 癌基因促进了许多人类癌症的发生。对其表达和功能的最新认识为治疗提供了机会。通过溴结构域蛋白激活 MYC 可以被类似药物的分子抑制,从而在体内抑制肿瘤。通过药理学方法使涉及葡萄糖或谷氨酰胺代谢的生物能量途径与 Myc 诱导的细胞生物量积累脱耦联,也可以抑制肿瘤生长。阻止 Myc 致癌的其他方法包括针对 Myc-Max 二聚化或 Myc 诱导的 microRNA 表达。本文综述了我们对 MYC 的丰富理解,强调了新的生物学见解和癌症治疗的机会。