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EGFR protects cancer cells from starvation via a kinase-independent mechanism
Date:5/5/2008

ncer cells are very active metabolically and consume more glucose than normal tissues; moreover, the EGFR overexpression and the associated enhanced stability of SGLT1 allow tumor cells to survive under conditions that would be less than optimal, even for normal cells.

Our results suggest that EGFR, independent of its kinase activity, maintains the basal intracellular glucose level and thereby prevents cancer cells from succumbing to autophagic death. It is possible that this function of the EGFR may even increase the survival capacity of cancer cells in the presence of chemotherapeutic agents, offers study author Dr. Mien-Chie Hung. The researchers suggest that inhibition of both EGFR-mediated SGLT1 stabilization and EGFR kinase activity may be necessary for eradication of epithelial tumors.


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Contact: Cathleen Genova
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