Epidermal Growth Factor Promotes Protein Degradation of Epithelial Protein Lost in Neoplasm (EPLIN), a Putative Metastasis Suppressor, during Epithelial-mesenchymal Transition

• Type of Material: Article
• Authors: Shumin Zhang, Emory University; Xu Wang, Emory University; Shareen Iqbal, Emory University; Yanru Wang, Emory University; Adeboye O. Osunkoya, Emory University; Zhengjia Chen, Emory University; Zhuo Chen, Emory University; Dong M Shin, Emory University; Hongwei Yuan, Inner Mongolia Medical College; Yongqiang A. Wang, Ocean NanoTech, LLC; Haiyen E. Zhau, Cedars-Sinai Medical Center; Leland W. K. Chung, Cedars-Sinai Medical Center; Chad Ritenour, Emory University; Omer Kucuk, Emory University; Daqing Wu, Emory University
• Language: English
• Date: 2013-01-18
• Publisher: American Society for Biochemistry and Molecular Biology
• Publication Version: Final Published Version
• Copyright Statement: © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.
• Final Published Version (URL): http://www.jbc.org/content/288/3/1469
• Title of Journal or Parent Work: Journal of Biological Chemistry
• Volume: 288
• Issue: 3
• Start Page: 1469
• End Page: 1479
• Grant/Funding Information: This work was also supported by American Cancer Society Grant RSG-10-140-01 (to D. W.).; This work was supported, in whole or in part, by NCI, National Institutes of Health Grants 1R21CA164612-01A1 (to D. W), 1R43CA141870 (to Y. A. W), P01 CA098912 and R01 CA122602 (to L. W. K. C), and Georgia Cancer Coalition Distinguished Scholar Grant (to O. K).
• Keywords: EPLIN; Protein Turnover; Metastasis; Invasion; Prostate Cancer; Protein Phosphorylation; Protein Degradation; Epidermal Growth Factor (EGF); ERK; Epithelial to Mesenchymal Transition
• Research Categories: Health Sciences, Oncology; Chemistry, Biochemistry

Abstract

Background: The mechanism of EGF signaling in the regulation of prostate cancer (PCa) metastasis remains unclear. Results: EGF promotes epithelial-mesenchymal transition (EMT) and induces degradation of epithelial protein lost in neoplasm (EPLIN), a putative suppressor of PCa metastasis. Conclusion: EGF activates ERK1/2-dependent phosphorylation, ubiquitination, and protein turnover of EPLIN. Significance: This study suggested that blockade of EGF signaling could retard EMT and inhibit invasiveness of PCa cells.