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Effect of antisense VEGF cDNA transfection on the growth of chronic myeloid leukemia K562 cells in vitro and in nude mice
Ruan, GR; Liu, YR; Chen, SS; Fu, JY; Chang, Y; Qin, YZ; Li, JL; Yu, H; Wang, H
关键词Chronic Myeloid Leukemia Vascular Endothelial Growth Factor (Vegf) Transfection Proliferation Apoptosis
刊名LEUKEMIA RESEARCH
2004-07-01
DOI10.1016/j.leukres.2003.11.017
28期:7页:763-769
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Hematology
研究领域[WOS]Oncology ; Hematology
关键词[WOS]ACUTE LYMPHOBLASTIC-LEUKEMIA ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; CHRONIC MYELOGENOUS LEUKEMIA ; BONE-MARROW ANGIOGENESIS ; ENDOTHELIAL GROWTH ; MYELODYSPLASTIC SYNDROMES ; TUMOR ANGIOGENESIS ; MALIGNANCIES ; CML
英文摘要

To further elucidate the role of vascular endothelial growth factor (VEGF) in the pathogenesis of chronic myeloid leukemia (CML), we transfected K562 cells with a VEGF(121)cDNA sense vector (S), an antisense (AS) vector or vector (V) alone. The growth of transfected cells was investigated by MTT and colony-formation assays, and apoptosis was measured by flow cytometry (FCM) of Annexin-V-FITC/PI dual labeled cells. Transfected cells were subcutaneously transplanted into nude mice and the microvessel density (MVD) of tumor masses was determined by vWF immunohistochemistry staining. We tested the supernatant of different transfected K562 cells against human bone marrow endothelial cells (BMECs), and examined the synergic effects of antisense VEGF(121)cDNA and IFNalpha or STI571 on the proliferation and apoptosis of K562 cells. We found that K562/AS transfectants exhibited a 49% reduction in VEGF secretion, whereas K562/S transfectants exhibited a 3-fold increase in VEGF secretion, all in comparison to the vector controls. K562 cells transfected with antisense VEGF(121)cDNA showed growth retardation in vitro. In transplanted nude mice in vivo, transfection of implanted cells with antisense VEGF(121)cDNA resulted in decreased tumor MVD, and increased apoptosis in the presence of IFNalpha. Taken together, these results suggest that VEGF may be involved in the pathogenesis of CML through autocrine and paracrine mechanisms, and that anti-VEGF therapy alone or in combination with conventional treatment may be beneficial for CML patients. (C) 2004 Elsevier Ltd. All rights reserved.

语种英语
WOS记录号WOS:000221992200014
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被引频次:13[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55206
专题北京大学第二临床医学院_血液科
作者单位1.Peking Univ, Inst Hematol, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Beijing 100044, Peoples R China
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Ruan, GR,Liu, YR,Chen, SS,et al. Effect of antisense VEGF cDNA transfection on the growth of chronic myeloid leukemia K562 cells in vitro and in nude mice[J]. LEUKEMIA RESEARCH,2004,28(7):763-769.
APA Ruan, GR.,Liu, YR.,Chen, SS.,Fu, JY.,Chang, Y.,...&Wang, H.(2004).Effect of antisense VEGF cDNA transfection on the growth of chronic myeloid leukemia K562 cells in vitro and in nude mice.LEUKEMIA RESEARCH,28(7),763-769.
MLA Ruan, GR,et al."Effect of antisense VEGF cDNA transfection on the growth of chronic myeloid leukemia K562 cells in vitro and in nude mice".LEUKEMIA RESEARCH 28.7(2004):763-769.
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