Abstract
The DEAD-box family of RNA helicase is known to be required in virtually all cellular processes involving RNA, and p68 is a prototypic one of the family. Reports have indicated that in addition to ATPase and RNA helicase ability, p68 can also function as a co-activator for transcription factors such as estrogen receptor alpha, tumor suppressor p53 and beta-catenin. More than that, post-translational modification of p68 including phosphorylation, acetylation, sumoylation, and ubiquitylation can regulate the coactivation effect. Furthermore, aberrant expression of p68 in cancers highlights that p68 plays an important role for tumorgenesis and development. In this review, we briefly introduce the function and modulation of p68 in cancer cells, and put forward envisagement about future study about p68.
Highlights
The DEAD-box family of RNA helicases contains nine domains of strong peptide sequence conservation, including the Asp-Glu-Ala-Asp (DEAD) helicase signature sequence
In addition to regulating the conformation of RNA structure and the known ATP-dependent RNA helicase activity [1], DEAD box-containing proteins are required for a variety of processes involving RNA like ribosome biogenesis, embryogenesis, spermatogenesis, and cell development and division [2]
Many research studies demonstrated that p68 is important for a diverse range of cellular processes, including pre-mRNA, rRNA and miRNA processing and transcription [5]
Summary
The DEAD-box family of RNA helicases contains nine domains of strong peptide sequence conservation, including the Asp-Glu-Ala-Asp (DEAD) helicase signature sequence. SUMO modification is on a relative fixed site (K53) of p68, and can in bi-direction regulate its transcriptional repression activity and the ability as a co-activator of p53 [84] Both p68 and p72 can bind to the acetyltransferase p300, and the acetylation mediated by p300 resulted in aberrant activation of p68, promoting the interaction with HDACs [83]. Another documentation is the progressive increase of p68 expression level during the transition from polyp to adenoma, and to adenocarcinoma in colon [46] These details suggested that the RNA helicase p68 may play a vital role in regulating cancer cell grade and invasive potential. It has been reported that RNA helicase p68 is phosphorylated at tyrosine residue in cancer cells, compared with matched normal tissue, and the treatment of TNF-alpha and TRAIL (Tumor necrosis factor-related apoptosis-inducing ligand, an anticancer agent) would weaken the effect of phosphorylation [94]. With so many emerging implications of RNA helicase p68 in tumorgenesis and progression, we can demonstrate that p68 could be a potential target for cancer therapy
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