Survival of Cancer Cells Is Maintained by EGFR Independent of Its Kinase Activity

Expression of the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase associated with cell proliferation and survival, is overactive in many tumors of epithelial origin. Blockade of the kinase activity of EGFR has been used for cancer therapy; however, by itself, it does not seem to...

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Published inCancer cell Vol. 13; no. 5; pp. 385 - 393
Main Authors Weihua, Zhang, Tsan, Rachel, Huang, Wei-Chien, Wu, Qiuyu, Chiu, Chao-Hua, Fidler, Isaiah J., Hung, Mien-Chie
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.05.2008
Subjects
Autophagy
Cell Death
Cell Division
Cell Survival
CELLBIO
CELLCYCLE
Glucose - metabolism
Homeostasis
Humans
Kinetics
Neoplasm Metastasis
Neoplasms - pathology
Receptor Protein-Tyrosine Kinases - antagonists & inhibitors
Receptor Protein-Tyrosine Kinases - metabolism
Receptor, Epidermal Growth Factor - deficiency
Receptor, Epidermal Growth Factor - genetics
Receptor, Epidermal Growth Factor - physiology
RNA, Small Interfering - genetics
Sodium-Glucose Transporter 1 - physiology
CELLBIO
CELLCYCLE
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Summary:Expression of the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase associated with cell proliferation and survival, is overactive in many tumors of epithelial origin. Blockade of the kinase activity of EGFR has been used for cancer therapy; however, by itself, it does not seem to reach maximum therapeutic efficacy. We report here that in human cancer cells, the function of kinase-independent EGFR is to prevent autophagic cell death by maintaining intracellular glucose level through interaction and stabilization of the sodium/glucose cotransporter 1 (SGLT1).
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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Present address: Department of Urology, University of Pittsburgh Cancer Institute, University of Pittsburgh, 5200 Centre Avenue, Shadyside Medical Building, Ground Level 03, Pittsburgh, PA 15232, USA.
ISSN:1535-6108
1878-3686
DOI:10.1016/j.ccr.2008.03.015