Acridine Yellow G Blocks Glioblastoma Growth via Dual Inhibition of Epidermal Growth Factor Receptor and Protein Kinase C Kinases*

• Type of Material: Article
• Authors: Qi Qi, Emory University; Kunyan He, Emory University; Min-Heui Yoo, Emory University; Chi Bun Chan, Emory University; Xia Liu, Emory University; Zhaobin Zhang, Emory University; Jeffrey James Olson, Emory University; Ge Xiao, Centers for Disease Control and Prevention; Liya Wang, Emory University; Hui Mao, Emory University; Haian Fu, Emory University; Hui Tao, Emory University; Suresh S Ramalingam, Emory University; Shi-Yong Sun, Emory University; Paul S. Mischel, University of California Los Angeles; Keqiang Ye, Emory University
• Language: English
• Date: 2012-02-24
• Publisher: American Society for Biochemistry and Molecular Biology
• Publication Version: Final Published Version
• Copyright Statement: © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.
• Final Published Version (URL): http://www.jbc.org/content/287/9/6113
• Title of Journal or Parent Work: Journal of Biological Chemistry
• Volume: 287
• Issue: 9
• Start Page: 6113
• End Page: 6127
• Grant/Funding Information: This work was supported, in whole or in part, by National Institutes of Health Grant RO1 CA127119 (to K. Y.).
• Keywords: Drug Screening; Acridine Yellow G; Protein Kinase C (PKC); Signal Transduction; Cell Signaling; Anticancer Drug; EGFR; Glioblastoma; mTOR
• Research Categories: Health Sciences, Medicine and Surgery; Health Sciences, Pathology; Chemistry, Biochemistry

Abstract

Background: PTEN deletion renders glioblastomas resistant to epidermal growth factor receptor (EGFR) inhibitors. Results: Acridine yellow G inhibits both EGFR and PKCs, resulting in cell growth repression, cell cycle arrest in the G1 phase, and shrinkage of brain tumors. Conclusion: Acridine yellow G is a potent anti-tumor agent for malignant gliomas. Significance: Combinatorial inhibition of EGFR and PKCs provides the proof of concept for treating glioblastomas.