Mechanism of MYC Oncogene in Tumor Cell Proliferation

MYC proto-oncogene (MYC) is a well-known oncogene that can act as a transcription factor. Its abnormal activation can be observed in nearly all types of human malignant tumors. Inside tumor cells, MYC controls multiple biological events including cell cycle progression, DNA replication, glycolysis and glutamine metabolism. By regulating these processes, it pushes tumor cells to divide continuously and reshapes cellular metabolism, making it a viable target for cancer therapy. This paper first introduces MYC’s protein structure and core biological roles, then explores its mechanisms driving tumor formation and progression. Previous studies results have identified two main ways for MYC to drive tumor proliferation. First, MYC binds MYC-associated factor X (MAX) to form protein dimers, then regulates target genes to speed up the shift from G1 to S phase and DNA replication. In this way, tumor cells break the growth limits that normal cells follow. Second, MYC rewrites glucose and glutamine metabolism to supply enough energy and raw materials for cell division. Scientists have come up with several ways to block MYC’s activity that cause cancer. These include disrupting the MYC-MAX binding, lowering MYC levels, speeding up MYC protein degradation, and interfering with glycolysis and glutamine metabolism controlled by MYC. Recent studies also indicate that MYC can alter the nutrient composition inside tumor microenvironment, which provides new research direction for combining MYC inhibitors with immunotherapy. MYC links uncontrolled tumor growth and metabolic changes in tumors, so therapies targeting this gene shows great clinical potential. However, most relevant research only stays at cell and animal preclinical stages. Future research needs to focus on improving drug selectivity and safety, exploring how MYC works differently in various tissue cells, and advancing lab discoveries into clinical treatments.