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The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an "undruggable" target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors.
Bamrah et al. (Fri,) studied this question.