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Tristetraprolin suppresses AHRR expression through mRNA destabilization
Author(s) -
Lee Hyun Hee,
Kim Won-Tae,
Kim Dong Hee,
Park Jeong Woo,
Kang Tae-Hong,
Chung Jin Woong,
Leem Sun-Hee
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.03.031
Subject(s) - tristetraprolin , aryl hydrocarbon receptor , chemistry , messenger rna , repressor , microbiology and biotechnology , mutant , gene expression , untranslated region , transcription (linguistics) , transcription factor , gene , biochemistry , biology , linguistics , philosophy
The aryl hydrocarbon receptor repressor (AHRR) inhibits the transcription of the aryl hydrocarbon receptor (AHR) by binding to XRE. We report that AHRR expression is inhibited by tristetraprolin (TTP), an AU‐rich element (ARE)‐binding protein. Overexpression of TTP decreased the mRNA stability and protein expression of AHRR, and TTP‐overexpressing cells made smaller colonies than the control. Contrarily, inhibition of TTP by siRNA increased AHRR expression. Analyses of point mutants of the AREs demonstrated that AREs were responsible for the TTP‐mediated destabilization of AHRR mRNA. RNA EMSA revealed that TTP directly binds to the AHRR 3′UTR. Taken together, we demonstrate that TTP acts as a negative regulator of AHRR and may affect tumor development through induction of tumor suppressor genes as observed in MDA‐MB435.