Triggering of Suicidal Erythrocyte Death by Regorafenib | Zendy

Jens Zierle | Zendy; Rosi Bissinger | Zendy; Ghada Bouguerra | Zendy; Salem Abbès | Zendy; Florian Läng | Zendy

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Triggering of Suicidal Erythrocyte Death by Regorafenib

Author(s) -

Jens Zierle,

Rosi Bissinger,

Ghada Bouguerra,

Salem Abbès,

Florian Läng

Publication year - 2016

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 - 10.1159/000438618

Subject(s) - regorafenib , phosphatidylserine , ceramide , annexin , apoptosis , chemistry , ionomycin , programmed cell death , microbiology and biotechnology , medicine , biophysics , pharmacology , endocrinology , biology , intracellular , biochemistry , phospholipid , membrane , colorectal cancer , cancer

The multikinase inhibitor regorafenib is utilized for the treatment of malignancy. The substance is effective in part by triggering suicidal death or apoptosis of tumor cells. Side effects of regorafenib include anemia. At least in theory, regorafenib induced anemia could result from stimulated suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i), oxidative stress and ceramide. The present study explored, whether regorafenib induces eryptosis and, if so, whether it is effective up- and/or downstream of Ca2+.

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