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Author Notes:

To whom correspondence should be addressed: 615 Michael St., Atlanta, GA 30300. Tel.: 404-712-2814; Fax: 404-712-9217; E-mail: kye@emory.edu.

Qi Qi and Kunyan He contributed equally to this work.

We thank M. Otten Reed for proofreading the manuscript.


Research Funding:

This work was supported, in whole or in part, by National Institutes of Health Grant RO1 CA127119 (to K. Y.).


  • Anticancer Drug
  • Cell Signaling
  • Drug Screening
  • mTOR
  • Protein Kinase C (PKC)
  • Signal Transduction
  • Acridine Yellow G
  • EGFR
  • Glioblastoma

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

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Journal Title:

Journal of Biological Chemistry


Volume 287, Number 9


, Pages 6113-6127

Type of Work:

Article | Final Publisher PDF


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.

Copyright information:

© 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

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