| Mechanism of Arsenic Trioxide Inhibiting Angiogenesis in Multiple Myeloma |
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| 作者姓名： | 王雅丹 胡豫 孙春艳 张小平 何文娟 |
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| 作者单位： | Institute of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China，Institute of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China，Institute of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China，Institute of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China，Institute of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China |
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| 基金项目： | ThisprojectwassupportedbyagrantfromtheNaturalSciecesFoundationofHubei,China(No.2003ABB017). |
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| 摘 要： | Duringthelast decade,the efficacy of arsenic tri-oxide(As2O3)in both newly diagnosed and relapsedpatients with acute promyelocytic leukemia(APL)hasbeen established.And now,As2O3is used with otheragentsintreating patients with relapsed and refractorymultiple myeloma(MM)in clinical practice1].Theinitial researches demonstratedthat As2O3couldinhibitproliferation andinduce apoptosisin MMcellsin vitroandin vivo2,3].In addition to affecting tumorgrowth,As2O3has been showntoinhibit angiogenes…
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| 关 键 词： | 三氧化砷 血管生成 骨髓瘤 病理机制 |
| 收稿时间： | 2005-04-25 |
Mechanisms of arsenic trioxide inhibiting angiogenesis in multiple myeloma |
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| Wang Yadan,Hu Yu,Sun Chunyan,Zhang Xiaoping,He Wenjuan.Mechanism of Arsenic Trioxide Inhibiting Angiogenesis in Multiple Myeloma[J].Journal of Zuazhong University of Science and Technology: Medical Edition,2006,26(1):43-46. |
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| Authors: | Wang Yadan Hu Yu Sun Chunyan Zhang Xiaoping He Wenjuan |
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| Institution: | Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan 430022, China |
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| Abstract: | In order to explore the molecular mechanism of arsenic trioxide treating multiple myeloma (MM) via inhibition of angiogenesis, the expression of brain derived neurotrophic factor (BDNF) and its specific receptor TrkB in human MM cell line KM3 and endothelial cell line ECV304 was detected by Western blotting. The angiogenic activity was evaluated by wound migration assay and tubule formation assay in vitro. The results showed that BDNF was detected in the MM cells and TrkB in the endothelial cells. Furthermore, 100 ng/mL BDNF could significantly induced endothelial cell tubule formation and wound migration. As_ 2 O_ 3 depressed the expression of BDNF and TrkB in the dose-and time-dependent manner. As_ 2 O_ 3 inhibited BDNF-induced wound migration and capillary tube formation. It was concluded that BDNF is a novel angiogenic protein as well as VEGF and has a relation with the pathogenesis of MM. As_ 2 O_ 3 interrupts a paracrine loop between MM cells and endothelial cells by down-regulating the TrkB expression in endothelial cells and inhibiting BDNF production in MM cells, finally resulting in inhibition of MM angiogenesis. This is probably one part of the mechanisms of the As_ 2 O_ 3 treating MM via the inhibition of angiogenesis. |
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| Keywords: | arsenic trioxide brain derived neurotrophic factor multiple myeloma angiogenesis |
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