Literature DB >> 26191229

Up-regulation of VEGF and its receptor in refractory leukemia cells.

Lei Wang1, Wenjun Zhang2, Yi Ding2, Bing Xiu2, Ping Li2, Yan Dong2, Qi Zhu1, Aibin Liang2.   

Abstract

OBJECTIVE: To analyze the causative mechanisms in refractory leukemia cells.
METHODS: Vascular endothelial growth factor (VEGF) blood plasma concentrations in 35 de novo, 6 relapse, 20 remission leukemia patients and 10 healthy kids were determined via ELISA analyses. Transcription levels of the VEGF receptors (VEGFR) Fms-like tyrosine kinase-1 (Flt-1) and kinase-domain insert containing receptor (KDR) were determined in participants' leucocytes with RT-PCR. Apoptosis rates as well as Cyt-C and Caspase-3 expression was determined in Jurkat, Jurkat(Bcl-2), healthy and recurrent leukemia leukocytes with and without VP-16 applications via flow cytometry. Total Akt (t-Akt) expression and its phosphorylation (p-AKT) status in leukocytes of the participants were analyzed with western blots.
RESULTS: Healthy children and the remission group had the lowest blood plasma VEGF concentrations (91.16±41.34 vs. 135.80±111.28 pg/ml), followed by de novo leukemia patients (362.49±195.68 pg/ml-494.19±186.23 pg/ml) and relapse patients (574.37±278.45 pg/ml) (P<0.01). The same trend was statistically significant visible for Flt-1 and KDR expressions in leukocytes of the participants. Stable Bcl-2 overexpression led to reduced apoptosis rates as well as Cyt-C and Caspase-3 expressions in Jurkat cells after VP-16 application, which was similar in leucocytes of remission patients. In contrast to no phosphorylation in healthy children, Akt was phosphorylated in 10% remission samples, 30% de novo leukemia samples and in 67% of recurrent leukemia leucocytes.
CONCLUSION: High VEGF plus VEGFR expression and AKT phosphorylation are highest in leukocytes of remission patients, suggesting VEGF signaling as a cause of reduced apoptosis susceptibility upon treatments.

Entities:  

Keywords:  Flt-1; KDR; PI3K/AKT; VEGF; apoptosis; leukemia

Mesh:

Substances:

Year:  2015        PMID: 26191229      PMCID: PMC4503100     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


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