Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 445, Issue 4, Pages 795-801Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2014.02.022
Keywords
Acidic fibroblast growth factor; Phage display; Proliferation; Cell cycle; Breast cancer
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Funding
- Guangzhou Science & Technology Project [2010Y1-C541]
- 211 Project
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It has been reported that acidic fibroblast growth factor (aFGF) is expressed in breast cancer and via interactions with fibroblast growth factor receptors (FGFRs) to promote the stage and grade of the disease. Thus, aFGF/FGFRs have been considered essential targets in breast cancer therapy. We identified a specific aFGF-binding peptide (AGNWTPI, named AP8) from a phage display heptapeptide library with aFGF after four rounds of biopanning. The peptide APE contained two (TP) amino acids identical and showed high homology to the peptides of the 182-188 (GTPNPTL) site of high-affinity aFGF receptor FGFRI. Functional analyses indicated that APE specifically competed with the corresponding phage clone A8 for binding to aFGF. In addition, AP8 could inhibit aFGF-stimulated cell proliferation, arrested the cell cycle at the GO/G1 phase by increasing PA2G4 and suppressing Cyclin D1 and PCNA, and blocked the aFGF-induced activation of Erkl /2 and Akt kinase in both breast cancer cells and vascular endothelial cells. Therefore, these results indicate that peptide APE, acting as an aFGF antagonist, is a promising therapeutic agent for the treatment of breast cancer. (c) 2014 Elsevier Inc. All rights reserved.
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