Abstract
Myelocytomatosis oncogene (MYC) family members, including cellular MYC (c-Myc), neuroblastoma derived MYC (MYCN), and lung carcinoma derived MYC (MYCL), have all been implicated as key oncogenic drivers in a broad range of human cancers. Beyond cancer, MYC plays an important role in other physiological and pathological processes, namely immunity and immunological diseases. MYC largely functions as a transcription factor that promotes the expression of numerous target genes to coordinate death, proliferation, and metabolism at the cellular, tissue, and organismal levels. It has been shown that the expression of MYC family members is tightly regulated in immune cells during development or upon immune stimulations. Emerging evidence suggests that MYC family members play essential roles in regulating the development, differentiation and activation of immune cells. Through driving the expression of a broad range of metabolic genes in immune cells, MYC family members coordinate metabolic programs to support immune functions. Here, we discuss our understanding of MYC biology in immune system and how modulation of MYC impacts immune metabolism and responses.
Highlights
Cellular myelocytomatosis oncogene (C-Myelocytomatosis oncogene (MYC)) was the first Myc family member found in the human genome and was originally identified as a cellular homologue of the avian myelocytomatosis retroviral oncogene (v-Myc) [1,2]
It has been shown that 80% of the genes repressed by MXD1 have been found to be induced by MYC, postulating that cell proliferation may be controlled by the relative levels of MYC and MAX dimerization protein (MXD)-1 [38]
Accumulating evidence has demonstrated that MYC is a key regulator of many fundamental cellular processes in immune cells, most prominently of metabolic programs
Summary
Cellular myelocytomatosis oncogene (C-MYC) (referred to here as MYC) was the first Myc family member found in the human genome and was originally identified as a cellular homologue of the avian myelocytomatosis retroviral oncogene (v-Myc) [1,2]. MAX binds to members of the MAX dimerization protein (MXD) family through the. HLHZip region in the MYC bHLHZip domain completely abolish MYC’s functions in cells. Suggest that binding affinity for its partners and sub-nuclear localization patterns impact MYC’s mutations in the MYC bHLHZip domain completely abolish MYC’s functions in cells. TerminalMXD differentiation, inhibition of cell-cycle progression, impact functions MXD1, MXI1, MXD3, and MXD4 are associated terminal differentiation, inhibition of cell‐cycle bHLHZip transcription factor proteins, which in turn suppress mediated transformation progression, and tumor suppression [8,20]. MXD/MXI1 transformation and tumor growth [11,20]
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