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- Chien, Ming-Hsien (author)
Vascular endothelial growth factor-C (VEGF-C) promotes angiogenesis by induction of COX-2 in leukemic cells via the VEGF-R3/JNK/AP-1 pathway.
- Article/chapterEnglish2009
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- 2009-10-13
- Oxford University Press (OUP),2009
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- LIBRIS-ID:oai:DiVA.org:umu-106967
- https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-106967URI
- https://doi.org/10.1093/carcin/bgp244DOI
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- Language:English
- Summary in:English
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- Vascular endothelial growth factor (VEGF)-C is recognized as a tumor lymphangiogenic factor based on the effects of activated VEGF-R3 on lymphatic endothelial cells. Many tumor cells express VEGF-R3 but the function of this receptor in tumor cells is largely unknown. It has been reported that the VEGF-C/VEGF-R3 axis is activated in subsets of leukemia patients. Herein, we have shown that VEGF-C induces angiogenic activity in the tube formation assay invitro and Matrigel plug assay in vivo by upregulating an angiogenic factor, cyclooxygenase-2 (COX-2), through VEGF-R3 in the human acute myeloid leukemia (AML) cell line, THP-1. COX-2 induction by VEGF-C was also observed in other VEGF-R3(+) human AML cell lines (U937 and HL60). Moreover, immunohistochemical analysis of bone marrow specimens of 37 patients diagnosed with AML revealed that VEGF-C expression in specimens was associated with the expression of COX-2 (P < 0.001). The manner by which signaling pathways transduced by VEGF-C is responsible for COX-2 upregulation was further investigated. Blocking the p42/44 mitogen-activated protein kinase (MAPK) pathway with the MAPK kinase inhibitor, PD 98059, failed to inhibit VEGF-C-mediated COX-2 expression. However, VEGF-C-induced COX-2 upregulation was effectively abolished by overexpression of dominant-negative c-Jun N-terminal kinase (JNK) or treatment with the JNK inhibitor, SP 600125. VEGF-C induced JNK-dependent nuclear translocation of c-Jun. Furthermore, chromatin immunoprecipitation and reporter assays revealed that VEGF-C enhanced c-Jun binding to the cyclic adenosine 3',5'-monophosphate-response element of the COX-2 promoter and induced COX-2 expression. In sum, the data herein highlight the pathogenic role of VEGF-C in leukemia via regulation of angiogenesis through upregulation of COX-2.
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- Ku, Chia-Chi (author)
- Johansson, GunnarUmeå universitet,Onkologi,Umeå University(Swepub:umu)gurjon98 (author)
- Chen, Min-Wei (author)
- Hsiao, Michael (author)
- Su, Jen-Liang (author)
- Inoue, Hiroyasu (author)
- Hua, Kuo-Tai (author)
- Wei, Lin-Hung (author)
- Kuo, Min-Liang (author)
- Umeå universitetOnkologi (creator_code:org_t)
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- In:Carcinogenesis: Oxford University Press (OUP)30:12, s. 2005-130143-33341460-2180
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