Next Article in Journal
Immobilization of Laccase for Oxidative Coupling of Trans-Resveratrol and Its Derivatives
Previous Article in Journal
Multiplex PCR for 17 Y-Chromosome Specific Short Tandem Repeats (STR) to Enhance the Reliability of Fetal Sex Determination in Maternal Plasma
Article Menu

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2012, 13(5), 5982-5997; doi:10.3390/ijms13055982

The Role of Receptor for Advanced Glycation End Products (RAGE) in the Proliferation of Hepatocellular Carcinoma

1
Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha 410008, China
2
Medical Science Institute, Xiangya Hospital, Central South University, Changsha 410008, China
3
Immunogenetics Research Group, Department of Immunology, College of Basic Medical Sciences Central South University, Changsha 410013, China
4
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15219, USA
*
Author to whom correspondence should be addressed.
Received: 22 March 2012 / Revised: 9 May 2012 / Accepted: 14 May 2012 / Published: 18 May 2012
View Full-Text   |   Download PDF [284 KB, uploaded 19 June 2014]   |  

Abstract

The receptor for advanced glycation end products (RAGE) is oncogenic and overexpressed in human cancers, but its role in hepatocellular carcinoma remains unclear. Here we demonstrated that RAGE is overexpressed in primary hepatocellular carcinoma (PHC) compared to adjacent para-neoplastic liver samples. Serum endogenous secretory RAGE levels were also increased in PHC patients (p < 0.01). Moreover, we demonstrated that RAGE regulates cellular proliferation in Hepatocellular carcinoma (HCC). Knockdown of RAGE by specific siRNA inhibited cellular growth in the hepatocellular carcinoma cell line, Huh7, whereas the RAGE ligand, high mobility group box 1 protein (HMGB1) increased cellular proliferation. In addition, knockdown of RAGE by siRNA arrested cells in the G1 phase and inhibited DNA synthesis (p < 0.01), while HMGB1 protein decreased the number of cells in the G1 phase and increased the number in the S phase (p < 0.05). Furthermore, quantitative real time RT-PCR (qRT-PCR) and Western Blot results demonstrated that RAGE and HMGB1 positively regulate NF-κB p65 expression in Huh7 cells. These studies suggest that RAGE and RAGE ligands are important targets for therapeutic intervention in hepatocellular carcinoma. View Full-Text
Keywords: RAGE; HMGB1; siRNA; NF-κB; proliferation RAGE; HMGB1; siRNA; NF-κB; proliferation
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Yaser, A.-M.; Huang, Y.; Zhou, R.-R.; Hu, G.-S.; Xiao, M.-F.; Huang, Z.-B.; Duan, C.-J.; Tian, W.; Tang, D.-L.; Fan, X.-G. The Role of Receptor for Advanced Glycation End Products (RAGE) in the Proliferation of Hepatocellular Carcinoma. Int. J. Mol. Sci. 2012, 13, 5982-5997.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top