AJTR Copyright © 2009-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711
Am J Translational Res 2010;2(3):223-234

Review Article
Multi-talented DEAD-box proteins and potential tumor promoters: p68
RNA helicase (DDX5) and its paralog, p72 RNA helicase (DDX17)

Ralf Janknecht

Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, USA

Received April 17, 2010; accepted May 1, 2010, available online May 5, 2010

Abstract: P68 (DDX5) and p72 (DDX17) are members of the DEAD-box RNA helicase family. They can unwind
double-stranded RNA and also contribute to the remodeling of ribonucleoprotein complexes. These activities of
p68/p72 are required for efficient RNA splicing and microRNA processing. In addition, p68/p72 perform functions
that are independent of their enzymatic activity. This is especially common to their role in gene regulation, where
p68/p72 coactivate various transcription factors, including the tumor suppressor p53, estrogen receptor  and -
catenin. P68/p72 are posttranslationally modified by SUMO attachment and phosphorylation that regulate their
coactivation potential, binding to known interactants or protein stability. Knock-out mouse models revealed that
both DDX5 and DDX17 are essential genes during development. Furthermore, together with their ability to
stimulate cell proliferation and prevent apoptosis, the reported overexpression of p68/p72 in three of the major
human cancers (colon, breast, prostate), strongly suggests that p68/p72 promote tumorigenesis and might even
represent proto-oncoproteins. If so, their inhibition holds promise as a novel way to contain or cure various
carcinomas. (AJTR1004004).

Key words: Cancer, DDX5, DDX17, DEAD-box, p68 RNA helicase, p72 RNA helicase

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Address all correspondence to:
Ralf G. Janknecht
Department of Cell Biology
The University of Oklahoma Health Sciences Center
Biomedical Research Center BRC-1464
975 NE 10th Street
Oklahoma City, OK 73104, USA
E-mail:
ralf-janknecht@ouhsc.edu