Myc, consisting of 3 paralogs C-Myc, N-Myc and L-Myc, is a proto-oncogene. It functions as a universal transcription amplifier regulating nearly every physiological process in cells, such as cell cycle, proliferation, metabolism, differentiation, and apoptosis [2,3,7]. Myc is frequently deregulated in human cancers, playing a causal role in tumor initiation, maintenance, and progression [1,2,5,6].

In vivo studies show that Myc inhibition leads to a prominent anti-proliferative effect and sustained tumor regression in cancer, while any alteration on healthy tissue remains reversible [1]. Also, downregulation or inactivation of Myc impairs cell cycle progression as it regulates critical positive cell cycle regulators like Cdks, cyclins, and E2F transcription factors, and antagonizes cell cycle inhibitors [4]. In normal cells, Myc levels are tightly regulated, often through targeted degradation by the ubiquitin-proteasome system, and disruption of these regulatory mechanisms is associated with cancer [8].

In conclusion, Myc is a crucial regulator of multiple cellular processes. Its dysregulation is strongly linked to cancer. Research on Myc, especially through in vivo models demonstrating the impact of its inhibition, provides valuable insights into cancer biology, highlighting its potential as a therapeutic target for cancer treatment [1,2,5].