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Open AccessArticle

Histone Deacetylase Inhibitors Activate Tristetraprolin Expression through Induction of Early Growth Response Protein 1 (EGR1) in Colorectal Cancer Cells

Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA
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Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: André P. Gerber
Biomolecules 2015, 5(3), 2035-2055; https://doi.org/10.3390/biom5032035
Received: 21 May 2015 / Revised: 30 July 2015 / Accepted: 10 August 2015 / Published: 28 August 2015
(This article belongs to the Special Issue RNA-Binding Proteins—Structure, Function, Networks and Disease)
The RNA-binding protein tristetraprolin (TTP) promotes rapid decay of mRNAs bearing 3' UTR AU-rich elements (ARE). In many cancer types, loss of TTP expression is observed allowing for stabilization of ARE-mRNAs and their pathologic overexpression. Here we demonstrate that histone deacetylase (HDAC) inhibitors (Trichostatin A, SAHA and sodium butyrate) promote TTP expression in colorectal cancer cells (HCA-7, HCT-116, Moser and SW480 cells) and cervix carcinoma cells (HeLa). We found that HDAC inhibitors-induced TTP expression, promote the decay of COX-2 mRNA, and inhibit cancer cell proliferation. HDAC inhibitors were found to promote TTP transcription through activation of the transcription factor Early Growth Response protein 1 (EGR1). Altogether, our findings indicate that loss of TTP in tumors occurs through silencing of EGR1 and suggests a therapeutic approach to rescue TTP expression in colorectal cancer. View Full-Text
Keywords: HDAC; TTP; post-transcriptional regulation; COX-2; colon cancer HDAC; TTP; post-transcriptional regulation; COX-2; colon cancer
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Sobolewski, C.; Sanduja, S.; Blanco, F.F.; Hu, L.; Dixon, D.A. Histone Deacetylase Inhibitors Activate Tristetraprolin Expression through Induction of Early Growth Response Protein 1 (EGR1) in Colorectal Cancer Cells. Biomolecules 2015, 5, 2035-2055.

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