Effect of Autocrine VEGF on Chronic Myeloid Leukemia Cell Line K562
- Author:
Guo-Rui RUAN
1
;
Yan-Rong LIU
;
Shan-Shan CHEN
;
Ya-Zhen QIN
;
Hong YU
;
Yan CHANG
;
Jin-Lan LI
;
Jia-Yu FU
Author Information
1. Institute of Hematology and People Hospital, Peking University, Beijing 100044, China.
- Publication Type:Journal Article
- From:
Journal of Experimental Hematology
2001;9(3):202-206
- CountryChina
- Language:Chinese
-
Abstract:
Vascular endothelial growth factor (VEGF) is a specific mitogen for vascular endothelial cells. It has been associated with angiogenesis, growth, metastasis and poor prognosis in solid tumors. Lately, it has been known that VEGF expression is higher in bone marrow from chronic myeloid leukemia (CML) patients than that in normal subjects. However, it is not clarified that the effect of VEGF on the abnormal proliferation of CML cells. In order to explore the effect of autocrine VEGF on CML cells, K562 cells were transfected with the VEGF(121) cDNA sense vector (K562/S) or with the VEGF(121) cDNA antisense vector (K562/As). K562 cells were transfected with the pcDNA(3) vector (K562/V) as the control. Cell proliferation was determined by MTT and colony forming assay in vitro. Flow cytometric Annexin-V-FITC/PI dual labeling technique was performed to observe the effect of VEGF(121) cDNA transfection on apoptosis of K562 cells. Results indicated that K562/S transfectants exhibited a 3-fold increase in VEGF secretion, and K562/As transfectants exhibited a 49% reduction in VEGF secretion. K562/As showed a reduced growth rate and colony forming efficiency as compared to K562/V. K562/S showed an increasing growth rate and colony forming efficiency as compared to K562/V. K562/As had more apoptotic cells than K562/V and K562/S in the same culture condition. These data suggest that VEGF plays an important role in the abnormal proliferation and apoptosis in CML cells through an autocrine mechanism.
