| Literature DB >> 25892518 |
Masaya Kato1, Ryuta Muromoto1, Sumihito Togi1, Masashi Iwakami1, Yuichi Kitai1, Shigeyuki Kon1, Kenji Oritani2, Tadashi Matsuda3.
Abstract
The promyelocytic leukemia protein PML acts as a tumor suppressor by forming transcription-regulatory complexes with a variety of repressor proteins. In the present study, we found that endogenous PML suppresses interleukin (IL)-6-induced gene expression as well as phosphorylation and transcriptional activation of STAT3 in hepatoma cells. We also found that PML-mediated suppression of IL-6-induced STAT3 activation by disrupting interactions between STAT3 and HDAC3. These results indicate that PML modulates IL-6-induced STAT3 activation and hepatoma cell growth by interacting with HDAC3.Entities:
Keywords: HDAC3; Hepatoma; IL-6; PML; STAT3; Transcriptional regulation
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Year: 2015 PMID: 25892518 DOI: 10.1016/j.bbrc.2015.04.040
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575