Article: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma

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TitleIsolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma
AuthorsMa, NF1 4
Hu, L1
Fung, JM1
Xie, D2
Zheng, BJ1
Chen, L1
Tang, DJ1
Fu, L1
Wu, Z3
Chen, M1
Fang, Y2
Guan, XY1 2
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
CitationHepatology, 2008, v. 47 n. 2, p. 503-510 [How to Cite?]
DOI: http://dx.doi.org/10.1002/hep.22072
AbstractAmplification of 1q21 is the most frequent genetic alteration in human hepatocellular carcinoma (HCC), being detected in 58%-78% of primary HCC cases by comparative genomic hybridization. Recently, we isolated a candidate oncogene, Amplified in Liver Cancer 1 (ALC1), from 1q21 by hybrid selection. Here we demonstrate that ALC1 was frequently amplified and overexpressed in HCC. ALC1-transfected cells possessed a strong oncogenic ability, increasing the colony formation in soft agar and increasing the tumorigenicity in nude mice, which could be effectively suppressed by small interfering RNA against ALC1. Functional studies showed that overexpression of ALC1 could promote G1/S phase transition and inhibit apoptosis. Molecular studies revealed that the oncogenic function of ALC1 might be associated with its roles in promoting cell proliferation by down-regulating p53 expression. Conclusion: These results suggest that ALC1 is the target oncogene within the 1q21 amplicon and plays a pivotal role in HCC pathogenesis. Copyright © 2007 by the American Association for the Study of Liver Diseases.
ISSN0270-9139
2011 Impact Factor: 11.665
2011 SCImago Journal Rankings: 1.278
DOIhttp://dx.doi.org/10.1002/hep.22072
ISI Accession Number IDWOS:000252939500019
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorMa, NF
dc.contributor.authorHu, L
dc.contributor.authorFung, JM
dc.contributor.authorXie, D
dc.contributor.authorZheng, BJ
dc.contributor.authorChen, L
dc.contributor.authorTang, DJ
dc.contributor.authorFu, L
dc.contributor.authorWu, Z
dc.contributor.authorChen, M
dc.contributor.authorFang, Y
dc.contributor.authorGuan, XY
dc.date.accessioned2010-09-06T06:37:00Z
dc.date.available2010-09-06T06:37:00Z
dc.date.issued2008
dc.description.abstractAmplification of 1q21 is the most frequent genetic alteration in human hepatocellular carcinoma (HCC), being detected in 58%-78% of primary HCC cases by comparative genomic hybridization. Recently, we isolated a candidate oncogene, Amplified in Liver Cancer 1 (ALC1), from 1q21 by hybrid selection. Here we demonstrate that ALC1 was frequently amplified and overexpressed in HCC. ALC1-transfected cells possessed a strong oncogenic ability, increasing the colony formation in soft agar and increasing the tumorigenicity in nude mice, which could be effectively suppressed by small interfering RNA against ALC1. Functional studies showed that overexpression of ALC1 could promote G1/S phase transition and inhibit apoptosis. Molecular studies revealed that the oncogenic function of ALC1 might be associated with its roles in promoting cell proliferation by down-regulating p53 expression. Conclusion: These results suggest that ALC1 is the target oncogene within the 1q21 amplicon and plays a pivotal role in HCC pathogenesis. Copyright © 2007 by the American Association for the Study of Liver Diseases.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationHepatology, 2008, v. 47 n. 2, p. 503-510 [How to Cite?]
DOI: http://dx.doi.org/10.1002/hep.22072
dc.identifier.citeulike2937519
dc.identifier.doihttp://dx.doi.org/10.1002/hep.22072
dc.identifier.epage510
dc.identifier.hkuros146193
dc.identifier.isiWOS:000252939500019
dc.identifier.issn0270-9139
2011 Impact Factor: 11.665
2011 SCImago Journal Rankings: 1.278
dc.identifier.issue2
dc.identifier.openurl
dc.identifier.pmid18023026
dc.identifier.scopuseid_2-s2.0-39549087444
dc.identifier.spage503
dc.identifier.urihttp://hdl.handle.net/10722/71967
dc.identifier.volume47
dc.languageeng
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
dc.publisher.placeUnited States
dc.relation.ispartofHepatology
dc.relation.referencesReferences in Scopus
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.
dc.subject.meshCarcinoma, Hepatocellular - genetics - pathology
dc.subject.meshCell Line, Tumor
dc.subject.meshChromosomes, Human, Pair 1
dc.subject.meshGene Amplification
dc.subject.meshGene Expression Regulation, Neoplastic
dc.subject.meshGene Silencing
dc.subject.meshHumans
dc.subject.meshIn Situ Hybridization, Fluorescence
dc.subject.meshLiver Neoplasms - genetics - pathology
dc.subject.meshOncogene Proteins - genetics
dc.subject.meshOncogenes
dc.titleIsolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Sun Yat-Sen University
  3. Hong Kong University of Science and Technology
  4. Guangzhou Medical College