A common cancer gene works not by implementing unique gene-expression patterns as previously thought, but rather by boosting the expression of almost all active genes, according to work from two independent groups.
Increased expression of the gene MYC is often seen in human cancer, and generally bodes ill for prognosis. Richard Young at the Massachusetts Institute of Technology in Cambridge and his colleagues studied the encoded protein, c-Myc, in human tumour cells. The researchers found that c-Myc accumulates at the regulatory sequences of active genes and boosts their transcription into RNA, amplifying the gene-expression program already in place.
Meanwhile, Keji Zhao and David Levens at the National Institutes of Health in Bethesda, Maryland, and their colleagues analysed normal mouse cells. They showed that c-Myc did not induce gene expression itself, but rather amplified the expression of nearly all active genes.
This mechanism could help to explain the diverse effects of c-Myc in different cancers.