Translation, the synthesis of protein from an mRNA template, has long been considered a benign sequela to transcription. After all, dysregulation of transcription causes a multitude of human disorders, including cancer and metabolic diseases. But it turns out that translation is not so innocuous. Recent evidence has shown that dysregulation of two proteins involved in translation, eukaryotic initiation factor 4E (eIF4E) and the S6 kinases, contributes to carcinogenesis, for example. For this reason alone, translational regulation may be getting less attention than it should.
John Blenis, Harvard Medical School professor of cell biology, and colleagues helped rectify that. In the Nov. 18, 2005 Cell, they revealed just how S6 kinase 1 (S6K1) helps to regulate the initiation of protein synthesis. The findings not only fill a huge gap in the understanding of translation, but they may also lead to new insights into the development and treatment of cancer. “We are really excited about defining the molecular basis of translation initiation, but more importantly, the findings provide the real potential for developing biomarkers that can measure inappropriate activation of this signaling pathway in cancer and other diseases,” said Blenis.