PML suppresses IL-6-induced STAT3 activation by interfering with STAT3 and HDAC3 interaction.

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.

• Authors: Masaya Kato, Ryuta Muromoto, Sumihito Togi, Masashi Iwakami, Yuichi Kitai, Shigeyuki Kon, Kenji Oritani, Tadashi Matsuda
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 461 Issue 2 Pg. 366-71 (May 29 2015) ISSN: 1090-2104 [Electronic] United States
• PMID: 25892518 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier Inc. All rights reserved.

Chemical References

• Interleukin-6
• Nuclear Proteins
• Promyelocytic Leukemia Protein
• STAT3 Transcription Factor
• Transcription Factors
• Tumor Suppressor Proteins
• PML protein, human
• Histone Deacetylases
• histone deacetylase 3

Topics

• Carcinoma, Hepatocellular (genetics, metabolism)
• Cell Line, Tumor
• Gene Expression Regulation, Neoplastic
• Histone Deacetylases (metabolism)
• Humans
• Interleukin-6 (metabolism)
• Liver Neoplasms (genetics, metabolism)
• Nuclear Proteins (metabolism)
• Promyelocytic Leukemia Protein
• Protein Interaction Maps
• STAT3 Transcription Factor (genetics, metabolism)
• Transcription Factors (metabolism)
• Transcriptional Activation
• Tumor Suppressor Proteins (metabolism)