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Article: Down-regulation of tyrosine aminotransferase at a frequently deleted region 16q22 contributes to the pathogenesis of hepatocellular carcinoma

TitleDown-regulation of tyrosine aminotransferase at a frequently deleted region 16q22 contributes to the pathogenesis of hepatocellular carcinoma
Authors
Issue Date2010
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2010, v. 51 n. 5, p. 1624-1634 How to Cite?
AbstractLoss of 16q is one of the most frequent alterations in many malignancies including hepatocellular carcinomas (HCC), suggesting the existence of a tumor suppressor gene (TSG) within the frequently deleted region. In this report we describe the identification and characterization of one candidate TSG, tyrosine aminotransferase gene (TAT), at 16q22.1. Loss of one TAT allele was detected in 27/50 (54%) of primary HCCs by quantitative real-time polymerase chain reaction. In addition, homo-deletion of TAT alleles was detected in two cases. Down-regulation of TAT was detected in 28/50 (56%) of HCCs, which was significantly associated with the loss of TAT allele and hypermethylation of TAT 5′ CpG island (CGI) region (P < 0.001). Functional studies found that TAT has a strong tumor suppressive ability. Introduction of the TAT gene into HCC cell lines could effectively inhibit colony formation in soft agar, foci formation, and tumor formation in nude mice. Further study found that the tumor suppressive mechanism of TAT was associated with its proapoptotic role in a mitochondrial-dependent manner by promoting cytochrome-c release and activating caspase-9 and PARP. Conclusion: Taken together, our findings suggest that TAT plays an important suppressive role in the development and progression of HCC. Copyright © 2010 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/71965
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant CouncilHKU 7393/04M
Hong Kong Research Grant Council Central AllocationHKU 1/06C
HKU 5/CRF/08
Sun Yat-Sen University85000-3171311
Major State Basic Research Program of China2006CB910104
Funding Information:

Supported by Research Grant Council Grant (HKU 7393/04M), Hong Kong Research Grant Council Central Allocation (HKU 1/06C & HKU 5/CRF/08), Sun Yat-Sen University "Hundred Talents Program" (85000-3171311), and the Major State Basic Research Program of China (2006CB910104).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorFu, Len_HK
dc.contributor.authorDong, SSen_HK
dc.contributor.authorXie, YWen_HK
dc.contributor.authorTai, LSen_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorKong, KLen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorTao, Qen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-09-06T06:36:58Z-
dc.date.available2010-09-06T06:36:58Z-
dc.date.issued2010en_HK
dc.identifier.citationHepatology, 2010, v. 51 n. 5, p. 1624-1634en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71965-
dc.description.abstractLoss of 16q is one of the most frequent alterations in many malignancies including hepatocellular carcinomas (HCC), suggesting the existence of a tumor suppressor gene (TSG) within the frequently deleted region. In this report we describe the identification and characterization of one candidate TSG, tyrosine aminotransferase gene (TAT), at 16q22.1. Loss of one TAT allele was detected in 27/50 (54%) of primary HCCs by quantitative real-time polymerase chain reaction. In addition, homo-deletion of TAT alleles was detected in two cases. Down-regulation of TAT was detected in 28/50 (56%) of HCCs, which was significantly associated with the loss of TAT allele and hypermethylation of TAT 5′ CpG island (CGI) region (P < 0.001). Functional studies found that TAT has a strong tumor suppressive ability. Introduction of the TAT gene into HCC cell lines could effectively inhibit colony formation in soft agar, foci formation, and tumor formation in nude mice. Further study found that the tumor suppressive mechanism of TAT was associated with its proapoptotic role in a mitochondrial-dependent manner by promoting cytochrome-c release and activating caspase-9 and PARP. Conclusion: Taken together, our findings suggest that TAT plays an important suppressive role in the development and progression of HCC. Copyright © 2010 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshApoptosis - physiology-
dc.subject.meshCarcinoma, Hepatocellular - genetics-
dc.subject.meshDown-Regulation-
dc.subject.meshLiver Neoplasms - genetics-
dc.subject.meshTyrosine Transaminase - genetics-
dc.titleDown-regulation of tyrosine aminotransferase at a frequently deleted region 16q22 contributes to the pathogenesis of hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=51&issue=5&spage=1624&epage=1634&date=2010&atitle=Down-regulation+of+tyrosine+aminotransferase+at+a+frequently+deleted+region+16q22+contributes+to+the+pathogenesis+of+hepatocellular+carcinomaen_HK
dc.identifier.emailFu, L: gracelfu@hku.hken_HK
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.authorityFu, L=rp01435en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/hep.23540en_HK
dc.identifier.pmid20209601-
dc.identifier.scopuseid_2-s2.0-77951470463en_HK
dc.identifier.hkuros169979en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77951470463&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1624en_HK
dc.identifier.epage1634en_HK
dc.identifier.eissn1527-3350-
dc.identifier.isiWOS:000277261400020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10003309959-
dc.relation.projectCharacterization of roles of a novel oncogene ALC-1 in the development of hepatocellular carcinoma-
dc.relation.projectMolecular pathology of liver cancer - a multidisciplinary study-
dc.identifier.scopusauthoridFu, L=22979236700en_HK
dc.identifier.scopusauthoridDong, SS=35788109500en_HK
dc.identifier.scopusauthoridXie, YW=7403949124en_HK
dc.identifier.scopusauthoridTai, LS=7004457333en_HK
dc.identifier.scopusauthoridChen, L=23569135400en_HK
dc.identifier.scopusauthoridKong, KL=36106004300en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridLi, Y=36078824800en_HK
dc.identifier.scopusauthoridCheng, Y=8571459300en_HK
dc.identifier.scopusauthoridTao, Q=7102578359en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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