FAT 10, a gene up-regulated in various cancers, is cell-cycle regulated
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BioMed Central
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FAT10, a gene up-regulated in various cancers, is cell-cycle regulated Chuan-Bian Lim1, Dongwei Zhang2 and Caroline GL Lee*1,2 Address: 1Division of Medical Sciences, National Cancer Center, Singapore and 2Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Email: Chuan-Bian Lim - [email protected]; Dongwei Zhang - [email protected]; Caroline GL Lee* - [email protected] * Corresponding author
Published: 08 September 2006 Cell Division 2006, 1:20
doi:10.1186/1747-1028-1-20
Received: 13 July 2006 Accepted: 08 September 2006
This article is available from: http://www.celldiv.com/content/1/1/20 © 2006 Lim et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: FAT10 is a member of the ubiquitin-like-modifier family of proteins. Overexpression of the FAT10 gene was observed in the tumors of several epithelial cancers. High FAT10 expression was found to lead to increased chromosome instability via the reduction in the kinetochore localization of MAD2 during the prometaphase stage of the cell-cycle. FAT10 expression was also previously reported to be regulated by cytokines and p53. Results: Here, we report that FAT10 expression is regulated at the protein and transcript level during cell-cycle with highest expression observed during the S-phase of the cell-cycle. The distal region between -1997 to -975 bp from the transcription start site of the FAT10 promoter may play a role in the repression of FAT10 expression during G2/M phase of the cell-cycle. Conclusion: FAT10 expression is regulated during cell-cycle.
One of the hallmarks of cancer is the deregulation of cellcycle controls [1,2]. The cell-cycle is the timed sequence of events by which a cell duplicates all its components and produces two daughter cells. Successful progression through the cell cycle requires sequential activation of a variety of catalytic subunits called cyclin-dependent kinases (Cdks) that are dependent on the periodic synthesis of cell-cycle specific regulatory subunits known as cyclins [3]. The orderly transitions between the cell cycle phases are regulated by the proteolysis of cyclins; inhibitory phosphorylation of both Cdks and cyclins; as well as by the interaction with inhibitory regulators in a timely fashion [3]. Proteolytic destruction of cyclin proteins occurs through the 26S proteasome pathway, a process whereby each protein is covalently conjugated to an ubiquitin chain at one or more lysine residues, which serves as the signal for targeting the protein to the 26S proteasome for degradation [3,4]. Defects in the ubiquitin system can
lead to a plethora of diseases, including many cancers. For instance, MDM2, an ubiquitin ligase, was found to be amplified in human
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