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Its oncogenic effects depend on cellular context and influence multiple downstream pathways.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How can MYC inactivation lead to therapeutic benefit?",{"text":68,"@type":64},"Animal testing and clinical trials show that sustained tumor volume reduction can be achieved when MYC is inactivated. The review highlights targeting MYC-driven pathways as a way to delay cancerous growth and restore antitumor immune responses.",{"name":70,"@type":61,"acceptedAnswer":71},"Which MYC-associated complexes are discussed as potential treatment targets?",{"text":72,"@type":64},"The review highlights equilibrium points within the MYC/MAX, MIZ1/MYC/MAX, and MAD (MNT)/MAX complexes. 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Animal testing and clinical trials have shown that sustained tumor volume reduction can be achieved when MYC is inactivated, and different combinations of therapeutic agents including MYC inhibitors are currently being developed. In this review, we first provide a summary of the multiple biological functions of the MYC oncoprotein in cancer treatment, highlighting that the equilibrium points of the MYC/MAX, MIZ1/MYC/MAX, and MAD (MNT)/MAX complexes have further potential in cancer treatment that could be used to restrain MYC oncogene expression and its functions in tumorigenesis. We also discuss the multifunctional capacity of MYC in various cellular cancer processes, including its influences on immune response, metabolism, cell cycle, apoptosis, autophagy, pyroptosis, metastasis, angiogenesis, multidrug resistance, and intestinal flora. Moreover, we summarize the MYC therapy patent landscape and emphasize the potential of MYC as a druggable target, using herbal medicine modulators. Finally, we describe pending challenges and future perspectives in biomedical research, involving the development of therapeutic approaches to modulate MYC or its targeted genes. Patients with cancers driven by MYC signaling may benefit from therapies targeting these pathways, which could delay cancerous growth and recover antitumor immune responses.  \nKey words: MYC, cancer, immune response, multidrug resistance, natural product, herbal medicine  \n1. Introduction  \nMYC is a “global” transcription factor that contributes to various diseases, including cancers, age-associated disorders, and acute liver failure, among others. Due to its involvement in multiple cellular processes, including DNA repair, protein translation, cell cycle arrest, stress response, cellular proliferation and differentiation, programmed cell death, immune response regulation and  \nstem cell differentiation, MYC is referred to as a “master gene regulator”; it is thought to regulate approximately 15% of the human genome [1-4], and functions by controlling RNA polymerases to regulate transcription levels [5-7]. Among basic helix-loop-helix leucine zipper DNA binding proteins, c-MYC, N-MYC, and L-MYC comprise the MYC transcription factor (TF) subfamily, which is encoded on chromosome 8q24.21 (Fig. 1A) [8- 10] .  \nFigure 1. Schematic representations of the functional regions of three MYC paralogs. The N terminus of MYC comprises a transactivation domain locates on residues 1–143 and three highly conserved elements: MYC boxes (MB) 1–3 (MBI: residues 45-63; MBII: 128-143; MBIII: 169-199) . FBW7 targets the phosphodegron in MBI. MBII recruits a histone acetyltransferase (HAT) complex that mediates all known MYC functions. MBIII is key to regulating the stability and transcription level of MYC. The BR/HLH/LZ motif (residues 355-439) atthe C-terminus is necessary for DNA binding and binding to its canonical partner, MAX. (B) Summary of different classes of positive and negative regulatory factors that influence reg","cbCaibRfCjVhTzdz","https://ap.wps.com/l/cbCaibRfCjVhTzdz","pdf",2509948,58,"English","# Introduction\n## MYC as a master gene regulator\n## MYC paralogs and transcriptional mechanisms\n# MYC functions in cancer progression\n## Cellular context and downstream pathways\n## Immune regulation and immune evasion\n# MYC complexes as therapeutic leverage points\n## MYC/MAX, MIZ1/MYC/MAX, and MAD (MNT)/MAX\n# MYC-based natural product and herbal medicine strategies\n## Therapeutic patent landscape\n# Challenges and future perspectives\n## Developing MYC or target gene modulators","[{\"question\":\"What role does the MYC oncogene play in cancer?\",\"answer\":\"MYC is described as a “global” transcription factor involved in cancers and other disorders, and dysregulated MYC expression is associated with many human cancers. Its oncogenic effects depend on cellular context and influence multiple downstream pathways.\"},{\"question\":\"How can MYC inactivation lead to therapeutic benefit?\",\"answer\":\"Animal testing and clinical trials show that sustained tumor volume reduction can be achieved when MYC is inactivated. The review highlights targeting MYC-driven pathways as a way to delay cancerous growth and restore antitumor immune responses.\"},{\"question\":\"Which MYC-associated complexes are discussed as potential treatment targets?\",\"answer\":\"The review highlights equilibrium points within the MYC/MAX, MIZ1/MYC/MAX, and MAD (MNT)/MAX complexes. It notes that disrupting the balance among these complexes can affect transcriptional activity and cancer-related functions.\"}]","MYC Oncogene - Review - April 2024 | PDF",1789976276,146]