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Article: Effects of adrenaline in human colon adenocarcinoma HT-29 cells

TitleEffects of adrenaline in human colon adenocarcinoma HT-29 cells
Authors
KeywordsAdrenaline
Colon cancer
COX-2
Stress
Issue Date2011
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2011, v. 88 n. 25-26, p. 1108-1112 How to Cite?
AbstractAims: Stress has been implicated in the development of cancers. Adrenaline levels are increased in response to stress. The effects of adrenaline on colon cancer are largely unknown. The aims of the study are to determine the effects of adrenaline in human colon adenocarcinoma HT-29 cells and the possible underlying mechanisms involved. Main methods: The effect of adrenaline on HT-29 cell proliferation was determined by [ 3H] thymidine incorporation assay. Expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) were detected by Western blot. Matrix metalloproteinase-9 (MMP-9) activity and prostaglandin E 2 (PGE 2) release were determined by zymography and enzyme immunoassay, respectively. Key findings: Adrenaline stimulated HT-29 cell proliferation. This was accompanied by the enhanced expression of COX-2 and VEGF in HT-29 cells. Adrenaline also upregulated MMP-9 activity and PGE 2 release. Adrenaline stimulated HT-29 cell proliferation which was reversed by COX-2 inhibitor sc-236. COX-2 inhibitor also reverted the action of adrenaline on VEGF expression and MMP-9 activity. Further study was performed to determine the involvement of β-adrenoceptors. The stimulatory action of adrenaline on colon cancer growth was blocked by atenolol and ICI 118,551, a β 1- and β 2-selective antagonist, respectively. This signified the role of β-adrenoceptors in this process. In addition, both antagonists also abrogated the stimulating actions of adrenaline on COX-2, VEGF expression, MMP-9 activity and PGE 2 release in HT-29 cells. Significance: These results suggest that adrenaline stimulates cell proliferation of HT-29 cells via both β 1- and β 2-adrenoceptors by a COX-2 dependent pathway. © 2011 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/134853
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
Chinese University of Hong Kong
Hong Kong Research Grants CouncilCUHK 7499/05M
Funding Information:

The study was supported by the Committee on Research and Conference Grant of the University of Hong Kong, the Direct Grant for Research from the Chinese University of Hong Kong and the Hong Kong Research Grants Council (CUHK 7499/05M).

References

 

DC FieldValueLanguage
dc.contributor.authorWong, HPSen_HK
dc.contributor.authorHo, JWCen_HK
dc.contributor.authorKoo, MWLen_HK
dc.contributor.authorYu, Len_HK
dc.contributor.authorWu, WKKen_HK
dc.contributor.authorLam, EKYen_HK
dc.contributor.authorTai, EKKen_HK
dc.contributor.authorKo, JKSen_HK
dc.contributor.authorShin, VYen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2011-07-21T07:45:23Z-
dc.date.available2011-07-21T07:45:23Z-
dc.date.issued2011en_HK
dc.identifier.citationLife Sciences, 2011, v. 88 n. 25-26, p. 1108-1112en_HK
dc.identifier.issn0024-3205en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134853-
dc.description.abstractAims: Stress has been implicated in the development of cancers. Adrenaline levels are increased in response to stress. The effects of adrenaline on colon cancer are largely unknown. The aims of the study are to determine the effects of adrenaline in human colon adenocarcinoma HT-29 cells and the possible underlying mechanisms involved. Main methods: The effect of adrenaline on HT-29 cell proliferation was determined by [ 3H] thymidine incorporation assay. Expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) were detected by Western blot. Matrix metalloproteinase-9 (MMP-9) activity and prostaglandin E 2 (PGE 2) release were determined by zymography and enzyme immunoassay, respectively. Key findings: Adrenaline stimulated HT-29 cell proliferation. This was accompanied by the enhanced expression of COX-2 and VEGF in HT-29 cells. Adrenaline also upregulated MMP-9 activity and PGE 2 release. Adrenaline stimulated HT-29 cell proliferation which was reversed by COX-2 inhibitor sc-236. COX-2 inhibitor also reverted the action of adrenaline on VEGF expression and MMP-9 activity. Further study was performed to determine the involvement of β-adrenoceptors. The stimulatory action of adrenaline on colon cancer growth was blocked by atenolol and ICI 118,551, a β 1- and β 2-selective antagonist, respectively. This signified the role of β-adrenoceptors in this process. In addition, both antagonists also abrogated the stimulating actions of adrenaline on COX-2, VEGF expression, MMP-9 activity and PGE 2 release in HT-29 cells. Significance: These results suggest that adrenaline stimulates cell proliferation of HT-29 cells via both β 1- and β 2-adrenoceptors by a COX-2 dependent pathway. © 2011 Elsevier Inc. All rights reserved.en_HK
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_HK
dc.relation.ispartofLife Sciencesen_HK
dc.subjectAdrenalineen_HK
dc.subjectColon canceren_HK
dc.subjectCOX-2en_HK
dc.subjectStressen_HK
dc.titleEffects of adrenaline in human colon adenocarcinoma HT-29 cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0024-3205&volume=88&issue=25-26&spage=1108&epage=1112&date=2011&atitle=Effects+of+adrenaline+in+human+colon+adenocarcinoma+HT-29+cells-
dc.identifier.emailWong, HPS: hpswong@hkusua.hku.hken_HK
dc.identifier.emailKoo, MWL: wlkoo@hku.hken_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.authorityWong, HPS=rp00808en_HK
dc.identifier.authorityKoo, MWL=rp00233en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.lfs.2011.04.007en_HK
dc.identifier.pmid21565206-
dc.identifier.scopuseid_2-s2.0-79958054557en_HK
dc.identifier.hkuros186309-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79958054557&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume88en_HK
dc.identifier.issue25-26en_HK
dc.identifier.spage1108en_HK
dc.identifier.epage1112en_HK
dc.identifier.isiWOS:000291764100005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, HPS=8644138100en_HK
dc.identifier.scopusauthoridHo, JWC=7402649983en_HK
dc.identifier.scopusauthoridKoo, MWL=7004550899en_HK
dc.identifier.scopusauthoridYu, L=16314581700en_HK
dc.identifier.scopusauthoridWu, WKK=35323393800en_HK
dc.identifier.scopusauthoridLam, EKY=8644138600en_HK
dc.identifier.scopusauthoridTai, EKK=9842278900en_HK
dc.identifier.scopusauthoridKo, JKS=7402678571en_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridCho, CH=14067000400en_HK
dc.identifier.citeulike9252718-

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