Abstract

c-Myc (Myc) is oncoprotein and nuclear transcription factor which plays a crucial role in several central cellular processes, involving cell proliferation, transformation, inhibition of differentiation and apoptosis. These functions result from the transcriptional activity of Myc. To be a functional form, Myc protein binds to the Max which recruits the E-box. Dysregulated over-expression of Myc is observed in many human malignancies including breast cancer, small-cell lung cancer, osteosarcomas, glioblastomas, and myeloid leukemias. Therefore, inhibition of the Myc-Max dimerization is a promising strategy for anticancer therapy. In this review, we summarize the Myc-Max disruption by small molecules targeting the oncogene. These information will contribute to the research and development of Myc-targeted smallmolecule drugs.