Down-regulation of expression of vascular endothelial growth factor induced by arsenic trioxide in bone marrow cells of chronic myeloid leukemia.
- Author:
Li LI
1
;
Ri ZHANG
;
Zi-Ling ZHU
Author Information
1. Jiangsu Institute of Hematology, Department of Hematology, The First Affiliated Hospital of Suzhou University, Suzhou 215006, China.
- Publication Type:Journal Article
- MeSH:
Adolescent;
Adult;
Aged;
Arsenicals;
pharmacology;
Bone Marrow Cells;
drug effects;
metabolism;
Cells, Cultured;
Child;
Culture Media, Conditioned;
chemistry;
Down-Regulation;
drug effects;
Endothelial Growth Factors;
metabolism;
Enzyme-Linked Immunosorbent Assay;
Female;
Humans;
Intercellular Signaling Peptides and Proteins;
metabolism;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
blood;
pathology;
Lymphokines;
metabolism;
Male;
Middle Aged;
Oxides;
pharmacology;
Vascular Endothelial Growth Factor A;
Vascular Endothelial Growth Factors
- From:
Journal of Experimental Hematology
2003;11(3):263-265
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of arsenic trioxide (As(2)O(3)) on vascular endothelial growth factor (VEGF) expression in different courses of chronic myeloid leukemia (CML), VEGF level was measured with ELISA in the cultural supernatants of bone marrow mononuclear cells from CML patients. The results showed that supernatants of cultured bone marrow cells from 35 CML patients (20 chronic, 8 accelerated and 7 blast crisis phases) contained significantly higher VEGF levels (649.16 +/- 382.20 pg/ml, 560.27 +/- 409.14 pg/ml and 587.18 +/- 415.28 pg/ml, respectively) than that in 15 normal control samples (152.16 +/- 150.09 pg/ml; P < 0.01), but no significant differences were found in VEGF levels among different phases of CML. The bone marrow cells treated with As(2)O(3) (5 x 10(-6)mol/L) for 72 hours resulted in significant reduction of VEGF levels (down to 396.66 +/- 257.47 pg/ml, 363.42 +/- 239.85 pg/ml and 407.47 +/- 219.38 pg/ml, respectively) (P < 0.05). In conclusion, abnormal high expression of VEGF plays a role in the pathogenetic course of CML and it is probably an additional anticancer mechanism for As(2)O(3) to inhibit VEGF expression of leukemic cells.
