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Article: Serotonin metabolism is dysregulated in cholangiocarcinoma, which has implications for tumor growth

TitleSerotonin metabolism is dysregulated in cholangiocarcinoma, which has implications for tumor growth
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2008
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2008, v. 68 n. 22, p. 9184-9193 How to Cite?
AbstractCholangiocarcinoma is a devastating cancer of biliary origin with limited treatment options. Symptoms are usually evident after blockage of the bile duct by the tumor, and at this late stage, they are relatively resistant to chemotherapy and radiation therapy. Therefore, it is imperative that alternative treatment options are explored. We present novel data indicating that the metabolism of serotonin is dysregulated in cholangiocarcinoma cell lines, compared with normal cholangiocytes, and tissue and bile from cholangiocarcinoma patients. Specifically, there was an increased expression of tryptophan hydroxylase 1 and a suppression of monoamine oxidase A expression (enzymes responsible for the synthesis and degradation of serotonin, respectively) in cholangiocarcinoma. This resulted in an increased secretion of serotonin from cholangiocarcinoma and increased serotonin in the bile from cholangiocarcinoma patients. Increased local serotonin release may have implications on cholangiocarcinoma cell growth. Serotonin administration increased cholangiocarcinoma cell growth in vitro, whereas inhibition of serotonin synthesis decreases tumor cell growth both in vitro and in vivo. The data presented here represent the first evidence that serotonin metabolism is dysregulated in cholangiocarcinoma and that modulation of serotonin synthesis may represent an alternative target for the development of therapeutic strategies. © 2008 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/92502
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
NIHK01
DK078532
DK062975
DK58411
Veterans Affairs Merit Award
Veterans Affairs Research Scholar Award
MIUR2005067975_004
2006068958_001
2005067975_002
Funding Information:

Grant support: NIH K01 grant DK078532 (S. DeMorrow); Veterans Affairs Merit Award, Veterans Affairs Research Scholar Award, and NIH grants DK062975 and DK58411 (G. Alpini); MIUR grant 2005067975_004 (M. Marzioni); MIUR grant 2006068958_001 (Department of Gastroenterology, Universita Politecnica delle Marche, Ancona, Italy); MIUR grant PRIN 2005 and faculty funds (E. Gaudio); and MIUR grant 2005067975_002 (D. Alvaro).

References

 

DC FieldValueLanguage
dc.contributor.authorAlpini, Gen_HK
dc.contributor.authorInvernizzi, Pen_HK
dc.contributor.authorGaudio, Een_HK
dc.contributor.authorVenter, Jen_HK
dc.contributor.authorKopriva, Sen_HK
dc.contributor.authorBernuzzi, Fen_HK
dc.contributor.authorOnori, Pen_HK
dc.contributor.authorFranchitto, Aen_HK
dc.contributor.authorCoufal, Men_HK
dc.contributor.authorFrampton, Gen_HK
dc.contributor.authorAlvaro, Den_HK
dc.contributor.authorLee, SPen_HK
dc.contributor.authorMarzioni, Men_HK
dc.contributor.authorBenedetti, Aen_HK
dc.contributor.authorDeMorrow, Sen_HK
dc.date.accessioned2010-09-17T10:48:12Z-
dc.date.available2010-09-17T10:48:12Z-
dc.date.issued2008en_HK
dc.identifier.citationCancer Research, 2008, v. 68 n. 22, p. 9184-9193en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92502-
dc.description.abstractCholangiocarcinoma is a devastating cancer of biliary origin with limited treatment options. Symptoms are usually evident after blockage of the bile duct by the tumor, and at this late stage, they are relatively resistant to chemotherapy and radiation therapy. Therefore, it is imperative that alternative treatment options are explored. We present novel data indicating that the metabolism of serotonin is dysregulated in cholangiocarcinoma cell lines, compared with normal cholangiocytes, and tissue and bile from cholangiocarcinoma patients. Specifically, there was an increased expression of tryptophan hydroxylase 1 and a suppression of monoamine oxidase A expression (enzymes responsible for the synthesis and degradation of serotonin, respectively) in cholangiocarcinoma. This resulted in an increased secretion of serotonin from cholangiocarcinoma and increased serotonin in the bile from cholangiocarcinoma patients. Increased local serotonin release may have implications on cholangiocarcinoma cell growth. Serotonin administration increased cholangiocarcinoma cell growth in vitro, whereas inhibition of serotonin synthesis decreases tumor cell growth both in vitro and in vivo. The data presented here represent the first evidence that serotonin metabolism is dysregulated in cholangiocarcinoma and that modulation of serotonin synthesis may represent an alternative target for the development of therapeutic strategies. © 2008 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleSerotonin metabolism is dysregulated in cholangiocarcinoma, which has implications for tumor growthen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, SP: sumlee@hku.hken_HK
dc.identifier.authorityLee, SP=rp01351en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-08-2133en_HK
dc.identifier.pmid19010890-
dc.identifier.pmcidPMC2593938-
dc.identifier.scopuseid_2-s2.0-56449096956en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-56449096956&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume68en_HK
dc.identifier.issue22en_HK
dc.identifier.spage9184en_HK
dc.identifier.epage9193en_HK
dc.identifier.eissn1538-7445-
dc.identifier.isiWOS:000261136600013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridAlpini, G=7005824212en_HK
dc.identifier.scopusauthoridInvernizzi, P=6701743858en_HK
dc.identifier.scopusauthoridGaudio, E=7006542760en_HK
dc.identifier.scopusauthoridVenter, J=10145041300en_HK
dc.identifier.scopusauthoridKopriva, S=55407495000en_HK
dc.identifier.scopusauthoridBernuzzi, F=16400645400en_HK
dc.identifier.scopusauthoridOnori, P=6701535351en_HK
dc.identifier.scopusauthoridFranchitto, A=6701756460en_HK
dc.identifier.scopusauthoridCoufal, M=25651475500en_HK
dc.identifier.scopusauthoridFrampton, G=25651374700en_HK
dc.identifier.scopusauthoridAlvaro, D=7006353760en_HK
dc.identifier.scopusauthoridLee, SP=7601417497en_HK
dc.identifier.scopusauthoridMarzioni, M=6602452331en_HK
dc.identifier.scopusauthoridBenedetti, A=7202060237en_HK
dc.identifier.scopusauthoridDeMorrow, S=14031157400en_HK

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