Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX, USA.
Harold C. Simmons Comprehensive Cancer Center, UT Southwestern Medical Center, Dallas, TX, USA.
Small GTPases. 2020 Mar;11(2):86-94. doi: 10.1080/21541248.2017.1364821. Epub 2017 Nov 25.
Members of the MYC family of proto-oncogenes are the most commonly deregulated genes in all human cancers. MYC proteins drive an increase in cellular proliferation and facilitate multiple aspects of tumor initiation and progression, thereby controlling all hallmarks of cancer. MYC's ability to drive metabolic reprogramming of tumor cells leading to biomass accumulation and cellular proliferation is the most studied function of these oncogenes. MYC also regulates tumor progression and is often implicated in resistance to chemotherapy and in metastasis. While most oncogenic functions of MYC are attributed to its role as a transcription factor, more recently, new roles of MYC as a pro-survival factor in the cytoplasm suggest a previously unappreciated diversity in MYC's roles in cancer progression. This review will focus on the role of MYC in invasion and will discuss the canonical functions of MYC in Epithelial to Mesenchymal Transition and the cytoplasmic functions of MYC-nick in collective migration.
原癌基因家族成员 MYC 是所有人类癌症中最常见的失调基因。MYC 蛋白可促进细胞增殖,并促进肿瘤起始和进展的多个方面,从而控制癌症的所有特征。MYC 能够驱动肿瘤细胞的代谢重编程,导致生物量积累和细胞增殖,这是这些致癌基因最受研究的功能。MYC 还调节肿瘤进展,并且经常与化疗耐药和转移有关。虽然 MYC 的大多数致癌功能归因于其作为转录因子的作用,但最近,MYC 作为细胞质中存活因子的新作用表明,MYC 在癌症进展中的作用以前未被充分认识到。这篇综述将重点介绍 MYC 在侵袭中的作用,并讨论 MYC 在上皮间质转化中的经典功能和 MYC-nick 在集体迁移中的细胞质功能。