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Inhibition of K562 leukemia angiogenesis and growth by expression of antisense vascular endothelial growth factor
1State Key Laboratory of Experimental Hematology, Institute of Hematology & Hospital of Blood Diseases, Chinese Academy of Medical Sciences & Peking Union of Medical College, Tianjin 300020, China.
Abstract:
Vascular endothelial growth factor (VEGF), a major angiogenic factor, plays a key role in the growth of solid tumor. Recently, expression of VEGF and its receptors has been found on leukemic cells as well as on endothelial cells. VEGF may fulfill a fundamental role in promoting tumor angiogenesis and proliferation by stimulating both endothelial cells and leukemic cells. To investigate the role of VEGF in the angiogenesis and growth of leukemic cell, we used an antisense strategy to downregulate VEGF expression in K562 cells, a human erythroleukemia cell line. Expression of antisense-VEGF in K562 cells reduced the secretion of VEGF protein and inhibited cell survival. The proliferation and migration of human umbilical vein endothelial cells were decreased in response to the conditioned medium (CM) from K562 cells expressed antisense-VEGF, compared to CM from K562 cells transfected with vector control. Moreover, subcutaneous injection of nude mice with antisense-VEGF K562 cells inhibited tumor growth with a reduction of the density of microvessels and an increased apoptosis in those tumors, compared to vector control K562 cells. These results suggest that the efficient downregulation of the VEGF production in leukemic cells using antisense-VEGF may constitute a novel strategy of treatment in leukemia.
Insights
Downregulating vascular endothelial growth factor (VEGF) in leukemia cells inhibits cancer growth and blood vessel formation. This suggests antisense-VEGF is a potential novel treatment strategy for leukemia.
Area of Science:
- Oncology
- Molecular Biology
- Hematology
Background:
- Vascular endothelial growth factor (VEGF) is crucial for solid tumor angiogenesis and proliferation.
- VEGF and its receptors are expressed on both leukemic and endothelial cells, suggesting a role in leukemia.
- VEGF may stimulate both endothelial and leukemic cells, promoting tumor growth.
Purpose of the Study:
- To investigate the role of VEGF in leukemia angiogenesis and growth.
- To explore the potential of an antisense strategy to downregulate VEGF expression in K562 human erythroleukemia cells.
Main Methods:
- Utilized an antisense strategy to reduce VEGF expression in K562 leukemia cells.
- Assessed VEGF protein secretion, cell survival, and proliferation.
- Evaluated the impact of conditioned medium from modified K562 cells on human umbilical vein endothelial cell (HUVEC) migration and proliferation.
- Injected modified K562 cells into nude mice to assess tumor growth, microvessel density, and apoptosis in vivo.
Main Results:
- Antisense-VEGF expression in K562 cells significantly reduced VEGF protein secretion and inhibited cell survival.
- Conditioned medium from antisense-VEGF K562 cells decreased HUVEC proliferation and migration.
- Subcutaneous tumors in nude mice showed inhibited growth, reduced microvessel density, and increased apoptosis when injected with antisense-VEGF K562 cells compared to controls.
Conclusions:
- Efficient downregulation of VEGF production in leukemic cells via antisense-VEGF is feasible.
- Antisense-VEGF therapy demonstrates potential in inhibiting leukemia growth and angiogenesis.
- This approach represents a novel therapeutic strategy for leukemia treatment.
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