Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Cold Spring Harb Perspect Med. 2013 Nov 1;3(11):a014308. doi: 10.1101/cshperspect.a014308.
Since its discovery as an oncogene carried by the avian acute leukemia virus MC29 in myelocytomatosis (Roussel et al. 1979) and its cloning (Vennstrom et al. 1982), c-MYC (MYC), as well as its paralogs MYCN and MYCL1, has been shown to play essential roles in cycling progenitor cells born from proliferating zones during embryonic development, and in all proliferating cells after birth. MYC deletion induces cell-cycle exit or cell death, depending on the cell type and milieu, whereas MYC and MYCN amplification or overexpression promotes cell proliferation and occurs in many cancers. Here, we review the relationship of MYC family proteins to the four molecularly distinct medulloblastoma subgroups, discuss the possible roles MYC plays in each of these subgroups and in the developing cells of the posterior fossa, and speculate on possible therapeutic strategies targeting MYC.
自其作为髓母细胞瘤(Roussel 等人,1979 年)中的禽白血病病毒 MC29 携带的致癌基因而被发现以来,以及其被克隆(Vennstrom 等人,1982 年)以来,c-MYC(MYC)及其同系物 MYCN 和 MYCL1 已被证明在胚胎发育过程中从增殖区产生的循环祖细胞中以及出生后所有增殖细胞中发挥重要作用。MYC 的缺失会诱导细胞周期退出或细胞死亡,具体取决于细胞类型和环境,而 MYC 和 MYCN 的扩增或过表达则促进细胞增殖,并且发生在许多癌症中。在这里,我们回顾了 MYC 家族蛋白与四个分子上不同的髓母细胞瘤亚组之间的关系,讨论了 MYC 在这些亚组中的可能作用以及在后颅窝发育细胞中的作用,并推测了针对 MYC 的可能治疗策略。