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Article: Epinephrine stimulates esophageal squamous-cell carcinoma cell proliferation via β-adrenoceptor-dependent transactivation of extracellular signal-regulated kinase/cyclooxygenase-2 pathway

TitleEpinephrine stimulates esophageal squamous-cell carcinoma cell proliferation via β-adrenoceptor-dependent transactivation of extracellular signal-regulated kinase/cyclooxygenase-2 pathway
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
Citation
Journal Of Cellular Biochemistry, 2008, v. 105 n. 1, p. 53-60 How to Cite?
AbstractEsophageal cancer is the sixth leading causes of cancer-related death in the world. It is suggested that β-adrenoceptor is involved in the control of cell proliferation, but its role in the pathogenesis of esophageal cancer remains unknown. We therefore studied the role of β-adrenergic signaling in the regulation of growth of an esophageal squamous-cell carcinoma cell line HKESC-1. Results showed that both β1- and β2- adrenoceptors were expressed in HKESC-1 cells. Stimulation of β-adrenoceptors with epinephrine significantly increased HKESC-1 cell proliferation accompanied by elevation of intracellular cyclic AMP levels, which were abolished by β1- or β2-selective antagonists. Epinephrine also increased extracellular signal-regulated kinase-1/2 (ERK1/2) phosphorylation as well as cyclooxygenase-2 (COX-2) and cytosolic phospholipase A2 expression, which were blocked by β1- or β2-selective antagonists. Moreover, epinephrine increased cyclin D1, cyclin E2, cyclin-dependent kinase (CDK)-4, CDK-6, and E2F-1 expression and retinoblastoma protein phosphorylation at Ser807/811, all of which were abrogated by β1-adrenoceptor antagonist. Furthermore, epinephrine increased the expression of vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1 and -2 in a β2-adrenoceptor-, mitogen-activated protein kinase/ERK kinase (MEK)-, and COX-2-dependent manner. MEK or COX-2 inhibitor also significantly inhibited HKESC-1 cell proliferation induced by epinephrine. Collectively, we demonstrate that epinephrine stimulates esophageal squamous-cell carcinoma cell proliferation via β-adrenoceptor- dependent transactivation of ERK/COX-2 pathway. Stimulation of β1- and β2-adrenoceptors also elicits a differential response on the expression of cell cycle regulators. These novel findings may shed new light on the understanding of β-adrenergic signaling in the control of esophageal cancer cell growth. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/148580
ISSN
2015 Impact Factor: 3.446
2015 SCImago Journal Rankings: 1.520
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilCUHK 7565/06M
Funding Information:

Grant sponsor: Hong Kong Research Grants Council; Grant number: CUHK 7565/06M.

References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Xen_US
dc.contributor.authorWu, WKKen_US
dc.contributor.authorYu, Len_US
dc.contributor.authorSung, JJYen_US
dc.contributor.authorSrivastava, Gen_US
dc.contributor.authorZhang, STen_US
dc.contributor.authorCho, CHen_US
dc.date.accessioned2012-05-29T06:13:52Z-
dc.date.available2012-05-29T06:13:52Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Cellular Biochemistry, 2008, v. 105 n. 1, p. 53-60en_US
dc.identifier.issn0730-2312en_US
dc.identifier.urihttp://hdl.handle.net/10722/148580-
dc.description.abstractEsophageal cancer is the sixth leading causes of cancer-related death in the world. It is suggested that β-adrenoceptor is involved in the control of cell proliferation, but its role in the pathogenesis of esophageal cancer remains unknown. We therefore studied the role of β-adrenergic signaling in the regulation of growth of an esophageal squamous-cell carcinoma cell line HKESC-1. Results showed that both β1- and β2- adrenoceptors were expressed in HKESC-1 cells. Stimulation of β-adrenoceptors with epinephrine significantly increased HKESC-1 cell proliferation accompanied by elevation of intracellular cyclic AMP levels, which were abolished by β1- or β2-selective antagonists. Epinephrine also increased extracellular signal-regulated kinase-1/2 (ERK1/2) phosphorylation as well as cyclooxygenase-2 (COX-2) and cytosolic phospholipase A2 expression, which were blocked by β1- or β2-selective antagonists. Moreover, epinephrine increased cyclin D1, cyclin E2, cyclin-dependent kinase (CDK)-4, CDK-6, and E2F-1 expression and retinoblastoma protein phosphorylation at Ser807/811, all of which were abrogated by β1-adrenoceptor antagonist. Furthermore, epinephrine increased the expression of vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1 and -2 in a β2-adrenoceptor-, mitogen-activated protein kinase/ERK kinase (MEK)-, and COX-2-dependent manner. MEK or COX-2 inhibitor also significantly inhibited HKESC-1 cell proliferation induced by epinephrine. Collectively, we demonstrate that epinephrine stimulates esophageal squamous-cell carcinoma cell proliferation via β-adrenoceptor- dependent transactivation of ERK/COX-2 pathway. Stimulation of β1- and β2-adrenoceptors also elicits a differential response on the expression of cell cycle regulators. These novel findings may shed new light on the understanding of β-adrenergic signaling in the control of esophageal cancer cell growth. © 2008 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503en_US
dc.relation.ispartofJournal of Cellular Biochemistryen_US
dc.rightsJournal of Cellular Biochemistry. Copyright © John Wiley & Sons, Inc.-
dc.subject.meshAdrenergic Beta-Antagonists - Pharmacologyen_US
dc.subject.meshAgeden_US
dc.subject.meshCarcinoma, Squamous Cell - Genetics - Metabolism - Pathologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshCyclooxygenase 2 - Metabolismen_US
dc.subject.meshEpinephrine - Pharmacologyen_US
dc.subject.meshEsophageal Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Metabolismen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshGroup Iv Phospholipases A2 - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMap Kinase Signaling System - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPhosphorylation - Drug Effectsen_US
dc.subject.meshReceptors, Adrenergic, Beta - Genetics - Metabolismen_US
dc.subject.meshReceptors, Vascular Endothelial Growth Factor - Metabolismen_US
dc.subject.meshRetinoblastoma Protein - Metabolismen_US
dc.subject.meshTranscriptional Activation - Geneticsen_US
dc.subject.meshVascular Endothelial Growth Factor A - Metabolismen_US
dc.titleEpinephrine stimulates esophageal squamous-cell carcinoma cell proliferation via β-adrenoceptor-dependent transactivation of extracellular signal-regulated kinase/cyclooxygenase-2 pathwayen_US
dc.typeArticleen_US
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_US
dc.identifier.authoritySrivastava, G=rp00365en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jcb.21802en_US
dc.identifier.pmid18452159-
dc.identifier.scopuseid_2-s2.0-51849102803en_US
dc.identifier.hkuros150722-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51849102803&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume105en_US
dc.identifier.issue1en_US
dc.identifier.spage53en_US
dc.identifier.epage60en_US
dc.identifier.isiWOS:000259109200007-
dc.publisher.placeUnited Statesen_US

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