mRNA stability and cancer: an emerging link?
Many oncogenes, growth factor, cytokine and cell-cycle genes are regulated post-transcriptionally. The major mechanism is by controlling the rate of mRNA turnover for transcripts bearing destabilizing cis-elements. To date, only a handful of regulatory factors have been identified that appear to control a large pool of target mRNAs, suggesting that a slight perturbation in the control mechanism may generate wide-ranging effects that could contribute to the development of a complex disorder such as cancer. In support of this view, mRNA turnover responds to signalling pathways that are often overactive in cancer, suggesting a post-transcriptional component in addition to the well-recognised transcriptional aspect of oncogenesis. Here the authors review examples of deregulated post-transcriptional control in oncogenesis, discuss post-transcriptionally regulated transcripts of oncologic significance, and consider the key role of signalling pathways in linking both processes and as an enticing therapeutic prospect.
Benjamin
Don
D
Institute for Medical Microbiology, Petersplatz 10, 4001 Basel, Switzerland. Don.Benjamin@unibas.ch
Moroni
Christoph
C
D000818:Animals; D020029:Base Pairing; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D034502:Heterogeneous-Nuclear Ribonucleoprotein D / Q000378:metabolism; D006801:Humans; D051379:Mice; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism; D009374:Neoplasms, Experimental / Q000235:genetics / Q000378:metabolism; D009857:Oncogenes; D012323:RNA Processing, Post-Transcriptional; D020871:RNA Stability; D012333:RNA, Messenger / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics
D034502:Heterogeneous-Nuclear Ribonucleoprotein D; D012333:RNA, Messenger