Editorial Volume 7, Issue 7 pp 463—464

Stopping MYC in its tracks


Figure 1. Elevated levels of MYC-MAX complexes drive cell proliferation and carcinogenesis. The oncoprotein MYC and its dimerization partner MAX bind to specific DNA motifs (E-Box) and control the expression of a vast array of target genes. Elevated MYC levels reprogram target gene expression profiles which promote the cancer state. Small-molecule inhibitors of MYC-MAX protein-protein interaction reduce transcription factor binding to DNA and thus interfere with MYC-driven cancer cell proliferation.