VEGF Receptor Phosphorylation Status and Apoptosis is Modulated by a Green Tea Component, Epigallocatechin-3-gallate (EGCG) in B cell Chronic Lymphocytic Leukemia

摘要: We recently reported that chronic lymphocytic leukemia (CLL) cells synthesize and release vascular endothelial growth factor (VEGF) under normoxic hypoxic conditions. CLL B also express VEGF membrane receptors (VEGF-R1 VEGF-R2), suggesting they use as a survival factor. To assess the mechanism of apoptosis resistance related to VEGF, we determined impact on cells, studied epigallocatechin-3-gallate (EGCG), known receptor tyrosine kinase (RTK) inhibitor, status viability cells. VEGF165 significantly increased apoptotic immunoblotting revealed VEGF-R1 VEGF-R2 are spontaneously phosphorylated EGCG apoptosis/cell death in 8 10 samples measured by annexin V/propidium iodide (PI) staining. The increase V/PI staining was accompanied caspase-3 activation poly-adenosine diphosphate ribose polymerase (PARP) cleavage at low concentrations (3 microg/mL). Moreover, suppressed proteins B-cell leukemia/lymphoma-2 protein (Bcl-2), X-linked inhibitor (XIAP), myeloid cell leukemia-1 (Mcl-1) Finally, (3-25 microg/mL) phosphorylation, albeit incompletely. Thus, these results suggest signaling regulates signals interruption this autocrine pathway caspase subsequent leukemic death.