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- Publisher Website: 10.1002/hep.22072
- Scopus: eid_2-s2.0-39549087444
- PMID: 18023026
- WOS: WOS:000252939500019
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Article: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma
Title | 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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Authors | |
Issue Date | 2008 |
Publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/ |
Citation | Hepatology, 2008, v. 47 n. 2, p. 503-510 How to Cite? |
Abstract | Amplification 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. |
Persistent Identifier | http://hdl.handle.net/10722/71967 |
ISSN | 2023 Impact Factor: 12.9 2023 SCImago Journal Rankings: 5.011 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ma, NF | en_HK |
dc.contributor.author | Hu, L | en_HK |
dc.contributor.author | Fung, JM | en_HK |
dc.contributor.author | Xie, D | en_HK |
dc.contributor.author | Zheng, BJ | en_HK |
dc.contributor.author | Chen, L | en_HK |
dc.contributor.author | Tang, DJ | en_HK |
dc.contributor.author | Fu, L | en_HK |
dc.contributor.author | Wu, Z | en_HK |
dc.contributor.author | Chen, M | en_HK |
dc.contributor.author | Fang, Y | en_HK |
dc.contributor.author | Guan, XY | en_HK |
dc.date.accessioned | 2010-09-06T06:37:00Z | - |
dc.date.available | 2010-09-06T06:37:00Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Hepatology, 2008, v. 47 n. 2, p. 503-510 | en_HK |
dc.identifier.issn | 0270-9139 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/71967 | - |
dc.description.abstract | Amplification 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. | en_HK |
dc.language | eng | en_HK |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/ | en_HK |
dc.relation.ispartof | Hepatology | en_HK |
dc.rights | Hepatology. Copyright © John Wiley & Sons, Inc. | en_HK |
dc.subject.mesh | Carcinoma, Hepatocellular - genetics - pathology | en_HK |
dc.subject.mesh | Cell Line, Tumor | en_HK |
dc.subject.mesh | Chromosomes, Human, Pair 1 | en_HK |
dc.subject.mesh | Gene Amplification | en_HK |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | en_HK |
dc.subject.mesh | Gene Silencing | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | In Situ Hybridization, Fluorescence | en_HK |
dc.subject.mesh | Liver Neoplasms - genetics - pathology | en_HK |
dc.subject.mesh | Oncogene Proteins - genetics | en_HK |
dc.subject.mesh | Oncogenes | en_HK |
dc.title | Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=47&spage=503&epage=510&date=2008&atitle=Isolation+and+characterization+of+a+novel+oncogene,+amplified+in+liver+cancer+1,+within+a+commonly+amplified+region+at+1q21+in+hepatocellular+carcinoma. | en_HK |
dc.identifier.email | Zheng, BJ:bzheng@hkucc.hku.hk | en_HK |
dc.identifier.email | Fu, L:gracelfu@hku.hk | en_HK |
dc.identifier.email | Guan, XY:xyguan@hkucc.hku.hk | en_HK |
dc.identifier.authority | Zheng, BJ=rp00353 | en_HK |
dc.identifier.authority | Fu, L=rp01435 | en_HK |
dc.identifier.authority | Guan, XY=rp00454 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/hep.22072 | en_HK |
dc.identifier.pmid | 18023026 | - |
dc.identifier.scopus | eid_2-s2.0-39549087444 | en_HK |
dc.identifier.hkuros | 146193 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-39549087444&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 47 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 503 | en_HK |
dc.identifier.epage | 510 | en_HK |
dc.identifier.isi | WOS:000252939500019 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Ma, NF=35731661400 | en_HK |
dc.identifier.scopusauthorid | Hu, L=34770075600 | en_HK |
dc.identifier.scopusauthorid | Fung, JM=23469161200 | en_HK |
dc.identifier.scopusauthorid | Xie, D=35070710200 | en_HK |
dc.identifier.scopusauthorid | Zheng, BJ=7201780588 | en_HK |
dc.identifier.scopusauthorid | Chen, L=23569135400 | en_HK |
dc.identifier.scopusauthorid | Tang, DJ=12752134500 | en_HK |
dc.identifier.scopusauthorid | Fu, L=22979236700 | en_HK |
dc.identifier.scopusauthorid | Wu, Z=8218909600 | en_HK |
dc.identifier.scopusauthorid | Chen, M=13204327400 | en_HK |
dc.identifier.scopusauthorid | Fang, Y=7403457405 | en_HK |
dc.identifier.scopusauthorid | Guan, XY=7201463221 | en_HK |
dc.identifier.citeulike | 2937519 | - |
dc.identifier.issnl | 0270-9139 | - |