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Sunitinib-sensitive suicidal erythrocyte death.

Nazneen Shaik1, Adrian Lupescu, Florian Lang

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Sunitinib, a cancer drug, can induce eryptosis, a suicidal death in red blood cells. This occurs via increased calcium and caspase activation, even without cell nuclei or mitochondria.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Sunitinib is a multikinase inhibitor used to treat cancer by inducing apoptosis.
  • Eryptosis, or suicidal death of erythrocytes, can occur without nuclei or mitochondria, involving cell shrinkage and phosphatidylserine exposure.
  • Triggers for eryptosis include increased intracellular calcium, ceramide, ATP depletion, p38 kinase, and caspase activation.

Purpose of the Study:

  • To investigate whether sunitinib induces eryptosis in erythrocytes.
  • To elucidate the specific mechanisms by which sunitinib affects red blood cells.

Main Methods:

  • Erythrocytes were exposed to sunitinib (10 µM) for 48 hours.
  • Measurements included intracellular calcium ([Ca(2+)](i)), cell volume (forward scatter), phosphatidylserine exposure (annexin-V binding), and hemolysis.
  • Ceramide abundance and cytosolic ATP levels were also assessed.

Main Results:

  • Sunitinib significantly decreased cell volume and increased phosphatidylserine exposure and hemolysis.
  • A significant increase in intracellular calcium ([Ca(2+)](i)) was observed.
  • Sunitinib-induced effects were partially inhibited by removing extracellular calcium, p38 kinase inhibitor SB203580, and pancaspase inhibitor zVAD.
  • Sunitinib did not significantly alter ceramide or ATP levels.

Conclusions:

  • Sunitinib triggers eryptosis in erythrocytes, characterized by cell shrinkage, phosphatidylserine exposure, and hemolysis.
  • The process involves increased intracellular calcium, p38 kinase, and caspase activation.
  • Eryptosis can be induced by sunitinib independently of cellular nuclei and mitochondria.