Endostar, a modified recombinant human endostatin, suppresses angiogenesis through inhibition of Wnt/β-catenin signaling pathway
Endostar, a novel modified recombinant human endostatin, is now widely studied for the treatment of diseases that are characterized or caused by pathological angiogenesis. However, its molecular mechanism remains unclear. In this study, we investigated the effects of Endostar on the Wnt/β-catenin si...
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Published in | PloS one Vol. 9; no. 9; p. e107463 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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18.09.2014
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Abstract | Endostar, a novel modified recombinant human endostatin, is now widely studied for the treatment of diseases that are characterized or caused by pathological angiogenesis. However, its molecular mechanism remains unclear. In this study, we investigated the effects of Endostar on the Wnt/β-catenin signaling pathway, which has emerged as an important aspect of angiogenesis. We showed that Endostar significantly inhibited the proliferation, migration, invasion, and capillary-like tube formation of human umbilical vascular endothelial cells in a dose-dependent manner. Using a luciferase reporter assay, we also demonstrated that Endostar suppressed β-catenin-dependent T cell factor transcriptional activity in increasing doses. Moreover, we found that Endostar treatment also restricted the stabilized mutant β-catenin-mediated increase in transcriptional activity, suggesting that Endostar exerts its inhibitory influence on Wnt/β-catenin signaling by targeting β-catenin or its downstream molecules. Western blot and immunofluorescence results revealed that Endostar significantly decreased nuclear and total β-catenin levels. Finally, we discovered that Endostar down-regulated cyclin D1 and VEGF, two proteins that are known as the downstream targets of Wnt/β-catenin signaling and that also play important roles in angiogenesis. Our findings suggested that Endostar inhibits angiogenesis and that the downregulation of the Wnt/β-catenin signaling pathway may be involved in the inhibition of angiogenesis by Endostar. These results support the use of Endostar in further clinical applications. |
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AbstractList | Endostar, a novel modified recombinant human endostatin, is now widely studied for the treatment of diseases that are characterized or caused by pathological angiogenesis. However, its molecular mechanism remains unclear. In this study, we investigated the effects of Endostar on the Wnt/β-catenin signaling pathway, which has emerged as an important aspect of angiogenesis. We showed that Endostar significantly inhibited the proliferation, migration, invasion, and capillary-like tube formation of human umbilical vascular endothelial cells in a dose-dependent manner. Using a luciferase reporter assay, we also demonstrated that Endostar suppressed β-catenin-dependent T cell factor transcriptional activity in increasing doses. Moreover, we found that Endostar treatment also restricted the stabilized mutant β-catenin-mediated increase in transcriptional activity, suggesting that Endostar exerts its inhibitory influence on Wnt/β-catenin signaling by targeting β-catenin or its downstream molecules. Western blot and immunofluorescence results revealed that Endostar significantly decreased nuclear and total β-catenin levels. Finally, we discovered that Endostar down-regulated cyclin D1 and VEGF, two proteins that are known as the downstream targets of Wnt/β-catenin signaling and that also play important roles in angiogenesis. Our findings suggested that Endostar inhibits angiogenesis and that the downregulation of the Wnt/β-catenin signaling pathway may be involved in the inhibition of angiogenesis by Endostar. These results support the use of Endostar in further clinical applications. |
Author | Mao, Wei Wang, Lihui Wang, Haibing Huang, Zhaoquan Xu, Xiaoming Dai, Jin Zhuang, Qin Chen, Qian |
AuthorAffiliation | University of Regensburg, Germany 2 First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China 1 Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China |
AuthorAffiliation_xml | – name: 2 First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China – name: 1 Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China – name: University of Regensburg, Germany |
Author_xml | – sequence: 1 givenname: Xiaoming surname: Xu fullname: Xu, Xiaoming organization: Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China – sequence: 2 givenname: Wei surname: Mao fullname: Mao, Wei organization: Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China – sequence: 3 givenname: Qian surname: Chen fullname: Chen, Qian organization: First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China – sequence: 4 givenname: Qin surname: Zhuang fullname: Zhuang, Qin organization: First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China – sequence: 5 givenname: Lihui surname: Wang fullname: Wang, Lihui organization: First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China – sequence: 6 givenname: Jin surname: Dai fullname: Dai, Jin organization: Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China – sequence: 7 givenname: Haibing surname: Wang fullname: Wang, Haibing organization: Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China – sequence: 8 givenname: Zhaoquan surname: Huang fullname: Huang, Zhaoquan organization: Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China |
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Copyright | 2014 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2014 Xu et al 2014 Xu et al |
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Notes | Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: WM XMX ZQH. Performed the experiments: XMX QC QZ LHW JD HBW. Analyzed the data: XMX QC QZ. Contributed reagents/materials/analysis tools: XMX QC QZ LHW. Contributed to the writing of the manuscript: WM XMX. |
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SubjectTerms | Angiogenesis Atherosclerosis beta Catenin - antagonists & inhibitors Biology and Life Sciences Capillary tubes Cardiology Cell cycle Cell growth Cell Line Cell Movement - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Chinese medicine Clinical medicine Colorectal cancer Cyclin D1 Cyclin D1 - biosynthesis Diabetic retinopathy Downstream Endostatin Endostatins - pharmacology Endothelial cells Genes Hospitals Human Umbilical Vein Endothelial Cells - cytology Human Umbilical Vein Endothelial Cells - metabolism Humans Immunofluorescence Inhibition Kinases Lymphocytes T Medical treatment Medicine and Health Sciences Neovascularization, Pathologic - drug therapy Phosphorylation Proteins Recombinant Proteins - pharmacology Signal transduction Signaling Studies TCF Transcription Factors - antagonists & inhibitors Therapeutic applications Transcription, Genetic - drug effects Vascular endothelial growth factor Vascular Endothelial Growth Factor A - biosynthesis Wnt protein Wnt Proteins - antagonists & inhibitors Wnt Signaling Pathway - drug effects Wound Healing - drug effects β-Catenin |
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Title | Endostar, a modified recombinant human endostatin, suppresses angiogenesis through inhibition of Wnt/β-catenin signaling pathway |
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