| Literature DB >> 20116377 |
Ursula E Lee1, Zahra Ghiassi-Nejad, Andrew J Paris, Steven Yea, Goutham Narla, Martin Walsh, Scott L Friedman.
Abstract
The tumor suppressor Kruppel-like factor 6 (KLF6) is frequently inactivated in hepatocellular carcinoma (HCC). To unearth downstream transcriptional targets of KLF6, cDNA microarray analysis of whole liver was compared between KLF6+/+ and KLF6+/- mice. Pituitary tumor transforming gene 1 (PTTG1), an oncogene, was the most up-regulated transcript in KLF6+/- liver. In human HCCs, KLF6 mRNA was significantly decreased, associated with increased PTTG1. In HepG2, KLF6 transcriptionally repressed PTTG1 by direct promoter interaction. Whereas KLF6 downregulation by siRNA increased HepG2 proliferation, siRNA to PTTG1 was anti-proliferative. PTTG1 downregulation represents a novel tumor suppressor pathway of KLF6. Copyright (c) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.Entities:
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Year: 2010 PMID： 20116377 PMCID： PMC2827621 DOI： 10.1016/j.febslet.2010.01.049
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124