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Article: Berberine suppresses tumorigenicity and growth of nasopharyngeal carcinoma cells by inhibiting STAT3 activation induced by tumor associated fibroblasts

TitleBerberine suppresses tumorigenicity and growth of nasopharyngeal carcinoma cells by inhibiting STAT3 activation induced by tumor associated fibroblasts
Authors
Issue Date2013
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
Citation
BMC Cancer, 2013, v. 13, article no. 619 How to Cite?
AbstractBACKGROUND: Cortidis rhizoma (Huanglian) and its major therapeutic component, berberine, have drawn extensive attention in recent years for their anti-cancer properties. Growth inhibitory effects of berberine on multiple types of human cancer cells have been reported. Berberine inhibits invasion, induces cell cycle arrest and apoptosis in human cancer cells. The anti-inflammatory property of berberine, involving inhibition of Signal Transducer and Activator of Transcription 3 (STAT3) activation, has also been documented. METHODS: In this study, we have examined the effects of berberine on tumorigenicity and growth of nasopharyngeal carcinoma (NPC) cells and their relationship to STAT3 signaling using both in vivo and in vitro models. RESULTS: Berberine effectively inhibited the tumorigenicity and growth of an EBV-positive NPC cell line (C666-1) in athymic nude mice. Inhibition of tumorigenic growth of NPC cells in vivo was correlated with effective inhibition of STAT3 activation in NPC cells inside the tumor xenografts grown in nude mice. In vitro, berberine inhibited both constitutive and IL-6-induced STAT3 activation in NPC cells. Inhibition of STAT3 activation by berberine induced growth inhibition and apoptotic response in NPC cells. Tumor-associated fibroblasts were found to secret IL-6 and the conditioned medium harvested from the fibroblasts also induced STAT3 activation in NPC cells. Furthermore, STAT3 activation by conditioned medium of tumor-associated fibroblasts could be blocked by berberine or antibodies against IL-6 and IL-6R. CONCLUSIONS: Our observation that berberine effectively inhibited activation of STAT3 induced by tumor-associated fibroblasts suggests a role of berberine in modulating the effects of tumor stroma on the growth of NPC cells. The effective inhibition of STAT3 activation in NPC cells by berberine supports its potential use in the treatment of NPC.
Persistent Identifierhttp://hdl.handle.net/10722/198978
ISSN
2015 Impact Factor: 3.265
2015 SCImago Journal Rankings: 1.627
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTsang, CMen_US
dc.contributor.authorCheung, YCen_US
dc.contributor.authorLui, VWYen_US
dc.contributor.authorYip, YLen_US
dc.contributor.authorZhang, Gen_US
dc.contributor.authorLin, VWen_US
dc.contributor.authorCheung, KCPen_US
dc.contributor.authorFeng, Yen_US
dc.contributor.authorTsao, GSWen_US
dc.date.accessioned2014-07-22T00:58:48Z-
dc.date.available2014-07-22T00:58:48Z-
dc.date.issued2013en_US
dc.identifier.citationBMC Cancer, 2013, v. 13, article no. 619en_US
dc.identifier.issn1471-2407-
dc.identifier.urihttp://hdl.handle.net/10722/198978-
dc.description.abstractBACKGROUND: Cortidis rhizoma (Huanglian) and its major therapeutic component, berberine, have drawn extensive attention in recent years for their anti-cancer properties. Growth inhibitory effects of berberine on multiple types of human cancer cells have been reported. Berberine inhibits invasion, induces cell cycle arrest and apoptosis in human cancer cells. The anti-inflammatory property of berberine, involving inhibition of Signal Transducer and Activator of Transcription 3 (STAT3) activation, has also been documented. METHODS: In this study, we have examined the effects of berberine on tumorigenicity and growth of nasopharyngeal carcinoma (NPC) cells and their relationship to STAT3 signaling using both in vivo and in vitro models. RESULTS: Berberine effectively inhibited the tumorigenicity and growth of an EBV-positive NPC cell line (C666-1) in athymic nude mice. Inhibition of tumorigenic growth of NPC cells in vivo was correlated with effective inhibition of STAT3 activation in NPC cells inside the tumor xenografts grown in nude mice. In vitro, berberine inhibited both constitutive and IL-6-induced STAT3 activation in NPC cells. Inhibition of STAT3 activation by berberine induced growth inhibition and apoptotic response in NPC cells. Tumor-associated fibroblasts were found to secret IL-6 and the conditioned medium harvested from the fibroblasts also induced STAT3 activation in NPC cells. Furthermore, STAT3 activation by conditioned medium of tumor-associated fibroblasts could be blocked by berberine or antibodies against IL-6 and IL-6R. CONCLUSIONS: Our observation that berberine effectively inhibited activation of STAT3 induced by tumor-associated fibroblasts suggests a role of berberine in modulating the effects of tumor stroma on the growth of NPC cells. The effective inhibition of STAT3 activation in NPC cells by berberine supports its potential use in the treatment of NPC.-
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/-
dc.relation.ispartofBMC Canceren_US
dc.rightsBMC Cancer. Copyright © BioMed Central Ltd.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshBerberine - pharmacology - toxicity-
dc.subject.meshCell Transformation, Neoplastic - drug effects - metabolism-
dc.subject.meshFibroblasts - drug effects - metabolism-
dc.subject.meshNasopharyngeal Neoplasms - metabolism - pathology-
dc.subject.meshSTAT3 Transcription Factor - antagonists and inhibitors - metabolism-
dc.titleBerberine suppresses tumorigenicity and growth of nasopharyngeal carcinoma cells by inhibiting STAT3 activation induced by tumor associated fibroblastsen_US
dc.typeArticleen_US
dc.identifier.emailTsang, CM: anna0226@graduate.hku.hken_US
dc.identifier.emailCheung, YC: yccheuna@hkucc.hku.hken_US
dc.identifier.emailLui, VWY: vlui002@hku.hken_US
dc.identifier.emailYip, YL: elaineyip@graduate.hku.hken_US
dc.identifier.emailZhang, G: gtzhang@hku.hken_US
dc.identifier.emailFeng, Y: yfeng@hku.hken_US
dc.identifier.emailTsao, GSW: gswtsao@hku.hken_US
dc.identifier.authorityLui, VWY=rp01876en_US
dc.identifier.authorityFeng, Y=rp00466en_US
dc.identifier.authorityTsao, GSW=rp00399en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1471-2407-13-619-
dc.identifier.pmid24380387-
dc.identifier.pmcidPMC3890551-
dc.identifier.scopuseid_2-s2.0-84891368877-
dc.identifier.hkuros230729en_US
dc.identifier.volume13en_US
dc.identifier.isiWOS:000329843400001-
dc.publisher.placeUnited Kingdom-

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