| Aberrant expression and association of VEGF and Dll4/Notch pathway molecules under hypoxia in patients with lung cancer. | |
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MedLine Citation:
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PMID: 23275310 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Tumor angiogenesis plays important roles in the pathogenesis and prognosis of lung cancer. Both vascular endothelial growth factor (VEGF) and Dll4/Notch pathways are critical for angiogenesis, whereas their relationship under hypoxia in lung cancer remains unknown. Thus, in the present study, we evaluated the expression of VEGF and Dll4/Notch signaling molecules, and assessed their association with the microvessel density (CD31) and hypoxia (HIF1a) in lung cancer and normal lung tissues using immunohistochemical and Real-time RT-PCR techniques. Then, we investigated the biological function of Dll4 by transfecting Dll4 into HUVECs. In lung cancer tissues, Notch pathway molecules (HES1) and VEGF pathway molecules (VEGFR1 and VEGFR2) were significantly up-regulated, while the ratio of VEGFR1/VEGFR2 was decreased. CD31 and HIF1a were also found to be elevated in lung cancer. VEGFR1 was negatively correlated with Notch1 while positively correlated with Dll4. CD31 was positively correlated with HIF1a but negatively correlated with VEGFR1. Moreover, HIF1a was nearly positively correlated with HES1 in lung cancer tissues. After transfection, Dll4, Notch1 and VEGFR1 were up-regulated while VEGF and VEGFR2 were down-regulated in Dll4-transfected HUVECs compared with controls. Also, our findings suggest that the expression of VEGF and VEGFR2 increased gradually with the disease progression of lung cancer. In summary, VEGF and Notch signaling pathway molecules were overexpressed in lung cancer, which positively correlates with hypoxia (HIF1a) and angiogenesis (CD31). There might be a negative feedback loop between VEGF and Dll4/Notch signaling pathway in lung tumor angiogenesis. |
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Authors:
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S Yu; J Sun; J Zhang; X Xu; H Li; B Shan; T Tian; H Wang; D Ma; C Ji |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Histology and histopathology Volume: 28 ISSN: 1699-5848 ISO Abbreviation: Histol. Histopathol. Publication Date: 2013 Feb |
Date Detail:
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Created Date: 2012-12-31 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8609357 Medline TA: Histol Histopathol Country: Spain |
Other Details:
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Languages: eng Pagination: 277-84 Citation Subset: IM |
Affiliation:
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Department of Hematology, Qilu Hospital, Shandong University, Jinan, PR China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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