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Article: Suppression of Vascular Endothelial Growth Factor via Inactivation of Eukaryotic Elongation Factor 2 by Alkaloids in Coptidis rhizoma in Hepatocellular Carcinoma

TitleSuppression of Vascular Endothelial Growth Factor via Inactivation of Eukaryotic Elongation Factor 2 by Alkaloids in Coptidis rhizoma in Hepatocellular Carcinoma
Authors
Issue Date2014
PublisherSage Publications, Inc. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201510
Citation
Integrative Cancer Therapies, 2014, v. 13 n. 5, p. 425-434 How to Cite?
AbstractAim of study: To investigate the inhibitory effect of Coptidis rhizome aqueous extract (CRAE) on vascular endothelial growth factor (VEGF) expression and tumor angiogenesis in hepatocellular carcinoma (HCC). Methods: Quality control of CRAE was determined. Secretion of VEGF protein and expression of its mRNA in MHCC97L and Hep G2 cells were measured with enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction. Synthesis of nascent protein was determined by AHA-protein-labeling technologies. The in vivo antiangiogenic effect of CRAE was evaluated with a xenograft model. Results: Absence of organochlorine pesticides in CRAE was found, and phytochemical analysis showed that its components were in proportion of magnoflorine 2.2%, jatrorrhizine 1.68%, palmatine 4.4%, and berberine 13.8%. CRAE exhibited significant inhibition on VEGF secretion from MHCC97L and HepG2 cells at nontoxic doses. The mRNA transcripts of VEGF could not be inhibited by CRAE; however, synthesis of VEGF nascent protein was potently blocked by CRAE. CRAE intervention increased the phosphorylation of eukaryotic elongation factor 2 (eEF2) in HCC cells, which blocked eEF2 activity for proceeding nascent protein synthesis. The activity of eEF2 was restored in CRAE-treated HCC cells in the presence of A484594, leading to the recovery of VEGF expression. Berberine was found to be the major active component in CRAE; however, CRAE is more effective in inhibiting eEF2 activity compared to berberine treatment alone, suggesting the additive effect of other components present. Reduction of tumor size and neovascularization were observed in mice xenograft model. Conclusion: Our study postulates the antiangiogenic effect of CRAE on hepatocellular carcinoma via an eEF2-driven pathway.
Persistent Identifierhttp://hdl.handle.net/10722/193587
ISSN
2015 Impact Factor: 1.706
2015 SCImago Journal Rankings: 0.822
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTan, HYen_US
dc.contributor.authorWang, Nen_US
dc.contributor.authorTsao, GSWen_US
dc.contributor.authorZhang, Zen_US
dc.contributor.authorFeng, Yen_US
dc.date.accessioned2014-01-20T05:05:26Z-
dc.date.available2014-01-20T05:05:26Z-
dc.date.issued2014en_US
dc.identifier.citationIntegrative Cancer Therapies, 2014, v. 13 n. 5, p. 425-434en_US
dc.identifier.issn1534-7354-
dc.identifier.urihttp://hdl.handle.net/10722/193587-
dc.description.abstractAim of study: To investigate the inhibitory effect of Coptidis rhizome aqueous extract (CRAE) on vascular endothelial growth factor (VEGF) expression and tumor angiogenesis in hepatocellular carcinoma (HCC). Methods: Quality control of CRAE was determined. Secretion of VEGF protein and expression of its mRNA in MHCC97L and Hep G2 cells were measured with enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction. Synthesis of nascent protein was determined by AHA-protein-labeling technologies. The in vivo antiangiogenic effect of CRAE was evaluated with a xenograft model. Results: Absence of organochlorine pesticides in CRAE was found, and phytochemical analysis showed that its components were in proportion of magnoflorine 2.2%, jatrorrhizine 1.68%, palmatine 4.4%, and berberine 13.8%. CRAE exhibited significant inhibition on VEGF secretion from MHCC97L and HepG2 cells at nontoxic doses. The mRNA transcripts of VEGF could not be inhibited by CRAE; however, synthesis of VEGF nascent protein was potently blocked by CRAE. CRAE intervention increased the phosphorylation of eukaryotic elongation factor 2 (eEF2) in HCC cells, which blocked eEF2 activity for proceeding nascent protein synthesis. The activity of eEF2 was restored in CRAE-treated HCC cells in the presence of A484594, leading to the recovery of VEGF expression. Berberine was found to be the major active component in CRAE; however, CRAE is more effective in inhibiting eEF2 activity compared to berberine treatment alone, suggesting the additive effect of other components present. Reduction of tumor size and neovascularization were observed in mice xenograft model. Conclusion: Our study postulates the antiangiogenic effect of CRAE on hepatocellular carcinoma via an eEF2-driven pathway.-
dc.languageengen_US
dc.publisherSage Publications, Inc. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201510-
dc.relation.ispartofIntegrative Cancer Therapiesen_US
dc.rightsIntegrative Cancer Therapies. Copyright © Sage Publications, Inc..-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleSuppression of Vascular Endothelial Growth Factor via Inactivation of Eukaryotic Elongation Factor 2 by Alkaloids in Coptidis rhizoma in Hepatocellular Carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailWang, N: ckwang@hku.hken_US
dc.identifier.emailTsao, GSW: gswtsao@hku.hken_US
dc.identifier.emailZhang, Z: zhangzj@hkucc.hku.hken_US
dc.identifier.emailFeng, Y: yfeng@hku.hken_US
dc.identifier.authorityTsao, GSW=rp00399en_US
dc.identifier.authorityZhang, Z=rp01297en_US
dc.identifier.authorityFeng, Y=rp00466en_US
dc.description.naturepostprint-
dc.identifier.doi10.1177/1534735413513635en_US
dc.identifier.pmid24363282-
dc.identifier.scopuseid_2-s2.0-84906053371-
dc.identifier.hkuros227180en_US
dc.identifier.volume13-
dc.identifier.issue5-
dc.identifier.spage425-
dc.identifier.epage434-
dc.identifier.isiWOS:000340719500007-
dc.publisher.placeUnited States-

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