Cancer is a leading cause of death worldwide, resulting in ~10 million deaths in 2020. Major oncogenic effectors are the Myc proto-oncogene family, which consists of three members including c-Myc, N-Myc, and L-Myc. As a pertinent example of the role of the Myc family in tumorigenesis, amplification of MYCN in childhood neuroblastoma strongly correlates with poor patient prognosis. Complexes between Myc oncoproteins and their partners such as hypoxia-inducible factor-1α and Myc-associated protein X (MAX) result in proliferation arrest and pro-proliferative effects, respectively. Interactions with other proteins are also important for N-Myc activity. For instance, the enhancer of zest homolog 2 (EZH2) binds directly to N-Myc to stabilize it by acting as a competitor against the ubiquitin ligase, SCF^FBXW7, which prevents proteasomal degradation. Heat shock protein 90 may also be involved in N-Myc stabilization since it binds to EZH2 and prevents its degradation. N-Myc downstream-regulated gene 1 (NDRG1) is downregulated by N-Myc and participates in the regulation of cellular proliferation via associating with other proteins, such as glycogen synthase kinase-3β and low-density lipoprotein receptor-related protein 6. These molecular interactions provide a better understanding of the biologic roles of N-Myc and NDRG1, which can be potentially used as therapeutic targets. In addition to directly targeting these proteins, disrupting their key interactions may also be a promising strategy for anti-cancer drug development. This review examines the interactions between the Myc proteins and other molecules, with a special focus on the relationship between N-Myc and NDRG1 and possible therapeutic interventions.

癌症是全球主要死亡原因，2020 年将导致约 1000 万人死亡。主要致癌效应子是Myc原癌基因家族，由c-Myc、N-Myc和L-Myc 三个成员组成。作为 Myc 家族在肿瘤发生中的作用的一个相关例子，儿童神经母细胞瘤中MYCN的扩增与患者不良预后密切相关。Myc 癌蛋白与其伙伴（例如缺氧诱导因子 1 α ）之间的复合物Myc 相关蛋白 X (MAX) 分别导致增殖停滞和促增殖作用。与其他蛋白质的相互作用对于 N-Myc 活性也很重要。^{例如，zest 同源物 2 (EZH2) 的增强子直接与 N-Myc 结合，通过充当泛素连接酶 SCF FBXW7}的竞争者来稳定 N-Myc，从而防止蛋白酶体降解。热休克蛋白 90 也可能参与 N-Myc 稳定，因为它与 EZH2 结合并防止其降解。N-Myc 下游调节基因 1 (NDRG1) 被 N-Myc 下调，并通过与其他蛋白质（如糖原合酶激酶 3 β）结合参与细胞增殖的调节和低密度脂蛋白受体相关蛋白 6。这些分子相互作用使人们更好地了解 N-Myc 和 NDRG1 的生物学作用，它们可以作为潜在的治疗靶点。除了直接靶向这些蛋白质之外，破坏它们的关键相互作用也可能是抗癌药物开发的一个有前途的策略。这篇综述研究了 Myc 蛋白与其他分子之间的相互作用，特别关注 N-Myc 和 NDRG1 之间的关系以及可能的治疗干预措施。