Myc is the most frequent amplified oncogene in human cancers and its alteration is observed in a wide range of tumors, including breast, lung and prostate cancer. The mechanism by which c-Myc exerts its oncogenic functions is not completely clear and different hypothesis are still under investigation. The knowledge of the capacity of c-Myc to bind exclusively E-box sequences determined the discrepancy between genomic studies showing the binding of c-Myc to all active promoters and, on the other hand, the evidence that only 60% or less of the binding sites have E-box sequences.
In this review, Caforio et al. provide support to the hypothesis that the cooperation of c-Myc with transcriptional cofactors mediates c-Myc-induced cellular functions. The authors produce evidence that recently identified cofactors are involved in c-Myc control of survival mechanisms of cancer cells.
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