Open AccessTriggering of Suicidal Erythrocyte Death by Gefitinib
Author(s) -
Abdulla Al Mamun Bhuyan,
Teresa R. Wagner,
Hang Cao,
Florian Lang
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000471823
Subject(s) - gefitinib , phosphatidylserine , oxidative stress , apoptosis , endocrinology , medicine , biology , chemistry , microbiology and biotechnology , cancer research , epidermal growth factor receptor , pharmacology , biochemistry , receptor , phospholipid , membrane
The epidermal growth factor receptor-tyrosine kinase inhibitor gefitinib is effective against several malignancies and is mainly utilized in the treatment of epidermal growth factor receptor mutation positive non-small cell lung cancer. The anti-cancer effect of the drug involves stimulation of apoptosis. Side effects of gefitinib include anemia. At least in theory, the development of anemia during gefitinib treatment could result from triggering of eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling potentially stimulating eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i) and generation of oxidative stress. The present study explored, whether gefitinib stimulates eryptosis and, if so, whether its effect involves Ca2+ entry and/or oxidative stress.