DEAD box RNA helicase functions in cancer
- PMID: 23353573
- PMCID: PMC3590229
- DOI: 10.4161/rna.23312
DEAD box RNA helicase functions in cancer
Abstract
Members of the DEAD box family of RNA helicases are known to be involved in most cellular processes that require manipulation of RNA structure and, in many cases, exhibit other functions in addition to their established ATP-dependent RNA helicase activities. They thus play critical roles in cellular metabolism and in many cases have been implicated in cellular proliferation and/or neoplastic transformation. These proteins generally act as components of multi-protein complexes; therefore their precise role is likely to be influenced by their interacting partners and to be highly context-dependent. This may also provide an explanation for the sometimes conflicting reports suggesting that DEAD box proteins have both pro- and anti-proliferative roles in cancer.
Keywords: DEAD box; cancer; multifunctional RNA helicases; oncogene; tumor suppressor.
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References
-
- Abdelhaleem M. Do human RNA helicases have a role in cancer? Biochim Biophys Acta. 2004;1704:37–46. - PubMed
-
- George RE, Kenyon RM, McGuckin AG, Malcolm AJ, Pearson AD, Lunec J, United Kingdom Children’s Cancer Study Group Investigation of co-amplification of the candidate genes ornithine decarboxylase, ribonucleotide reductase, syndecan-1 and a DEAD box gene, DDX1, with N-myc in neuroblastoma. Oncogene. 1996;12:1583–7. - PubMed
-
- Squire JA, Thorner PS, Weitzman S, Maggi JD, Dirks P, Doyle J, et al. Co-amplification of MYCN and a DEAD box gene (DDX1) in primary neuroblastoma. Oncogene. 1995;10:1417–22. - PubMed
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