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Article: Dietary Compound Isoliquiritigenin Inhibits Breast Cancer Growth And Neoangiogenesis Via Blocking Vegf/vegfr-2 Signaling Pathway

TitleDietary Compound Isoliquiritigenin Inhibits Breast Cancer Growth And Neoangiogenesis Via Blocking Vegf/vegfr-2 Signaling Pathway
Authors
Issue Date2013
PublisherPlos. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2013, v. 8, p. 14 How to Cite?
AbstractAngiogenesis is crucial for cancer initiation, development and metastasis. Identifying natural botanicals targeting angiogenesis has been paid much attention for drug discovery in recent years, with the advantage of increased safety. Isoliquiritigenin (ISL) is a dietary chalcone-type flavonoid with various anti-cancer activities. However, little is known about the anti-angiogenic activity of isoliquiritigenin and its underlying mechanisms. Herein, we found that ISL significantly inhibited the VEGF-induced proliferation of human umbilical vein endothelial cells (HUVECs) at non-toxic concentration. A series of angiogenesis processes including tube formation, invasion and migration abilities of HUVECs were also interrupted by ISL in vitro. Furthermore, ISL suppressed sprout formation from VEGF-treated aortic rings in an ex-vivo model. Molecular mechanisms study demonstrated that ISL could significantly inhibit VEGF expression in breast cancer cells via promoting HIF-1α (Hypoxia inducible factor-1α) proteasome degradation and directly interacted with VEGFR-2 to block its kinase activity. In vivo studies further showed that ISL administration could inhibit breast cancer growth and neoangiogenesis accompanying with suppressed VEGF/VEGFR-2 signaling, elevated apoptosis ratio and little toxicity effects. Molecular docking simulation indicated that ISL could stably form hydrogen bonds and aromatic interactions within the ATP-binding region of VEGFR-2. Taken together, our study shed light on the potential application of ISL as a novel natural inhibitor for cancer angiogenesis via the VEGF/VEGFR-2 pathway. Future studies of ISL for chemoprevention or chemosensitization against breast cancer are thus warranted.
Persistent Identifierhttp://hdl.handle.net/10722/187876
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Zen_US
dc.contributor.authorWANG, Nen_US
dc.contributor.authorHan, Sen_US
dc.contributor.authorWang, Den_US
dc.contributor.authorMo, Sen_US
dc.contributor.authorYu, Len_US
dc.contributor.authorHuang, Hen_US
dc.contributor.authorTsui, Ken_US
dc.contributor.authorShen, Jen_US
dc.contributor.authorChen, Jen_US
dc.date.accessioned2013-08-21T07:16:33Z-
dc.date.available2013-08-21T07:16:33Z-
dc.date.issued2013en_US
dc.identifier.citationPlos One, 2013, v. 8, p. 14en_US
dc.identifier.urihttp://hdl.handle.net/10722/187876-
dc.description.abstractAngiogenesis is crucial for cancer initiation, development and metastasis. Identifying natural botanicals targeting angiogenesis has been paid much attention for drug discovery in recent years, with the advantage of increased safety. Isoliquiritigenin (ISL) is a dietary chalcone-type flavonoid with various anti-cancer activities. However, little is known about the anti-angiogenic activity of isoliquiritigenin and its underlying mechanisms. Herein, we found that ISL significantly inhibited the VEGF-induced proliferation of human umbilical vein endothelial cells (HUVECs) at non-toxic concentration. A series of angiogenesis processes including tube formation, invasion and migration abilities of HUVECs were also interrupted by ISL in vitro. Furthermore, ISL suppressed sprout formation from VEGF-treated aortic rings in an ex-vivo model. Molecular mechanisms study demonstrated that ISL could significantly inhibit VEGF expression in breast cancer cells via promoting HIF-1α (Hypoxia inducible factor-1α) proteasome degradation and directly interacted with VEGFR-2 to block its kinase activity. In vivo studies further showed that ISL administration could inhibit breast cancer growth and neoangiogenesis accompanying with suppressed VEGF/VEGFR-2 signaling, elevated apoptosis ratio and little toxicity effects. Molecular docking simulation indicated that ISL could stably form hydrogen bonds and aromatic interactions within the ATP-binding region of VEGFR-2. Taken together, our study shed light on the potential application of ISL as a novel natural inhibitor for cancer angiogenesis via the VEGF/VEGFR-2 pathway. Future studies of ISL for chemoprevention or chemosensitization against breast cancer are thus warranted.-
dc.languageengen_US
dc.publisherPlos. The Journal's web site is located at http://www.plosone.org/home.actionen_US
dc.relation.ispartofPlos Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleDietary Compound Isoliquiritigenin Inhibits Breast Cancer Growth And Neoangiogenesis Via Blocking Vegf/vegfr-2 Signaling Pathwayen_US
dc.typeArticleen_US
dc.identifier.emailWang, Z: wangzy@hku.hken_US
dc.identifier.emailShen, J: shenjg@hku.hken_US
dc.identifier.emailChen, J: abchen@hku.hken_US
dc.identifier.authorityShen, J=rp00487en_US
dc.identifier.authorityChen, J=rp01316en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0068566-
dc.identifier.pmcidPMC3702614-
dc.identifier.hkuros218167en_US
dc.identifier.volume8en_US
dc.identifier.spage14en_US
dc.identifier.epage14en_US

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