Post-transcriptional regulation in cancer.

Deregulation of gene expression is a hallmark of the cancer cell. Acquiring a new profile of expressed proteins may enable the cell to re-enter the cell cycle, or give them a growth or motility advantage over "normal cells". An efficient and rapid way to alter gene expression is via regulation of mRNAs already transcribed. Modifications of mRNA stability and/or translational efficiency are increasingly reported in cancer. mRNA stability and translation are controlled through a complex network of RNA/protein interactions involving recognition of specific target mRNAs by RNA-BPs. We review how alterations in regulatory sequences, RNA-BPs, or in upstream signalling pathways affect the stability and/or translational efficiency of mRNAs encoding proto-oncogenes, cytokines, cell cycle regulators and other regulatory proteins to promote tumorigenesis and cancer progression. A more thorough understanding of post-transcriptional mechanisms such as these will enable the design and development of specific therapies based on modulating the translation or stability of specific mRNAs. Copyright 2004 Elsevier SAS