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Article: Granulin-epithelin precursor overexpression promotes growth and invasion of hepatocellular carcinoma

TitleGranulin-epithelin precursor overexpression promotes growth and invasion of hepatocellular carcinoma
Authors
Issue Date2004
Citation
Clinical Cancer Research, 2004, v. 10 n. 22, p. 7629-7636 How to Cite?
AbstractPurpose: Granulin-epithelin precursor (GEP) is a novel growih factor. Our earlier cDNA microarray study indicated that GEP was overexpressed in hepatocellular carcinoma (HCC). The aim of this study was to investigate the clinical significance of GEP expression and its potential as a therapeutic target in HCC. Experimental Design: A total of 110 pairs of HCCs and adjacent nontumor liver tissues, and 22 normal liver tissues were examined. The GEP RNA level was examined by quantitative reverse transcription-PCR, and protein localization by immunohistochemistry. The GEP function was examined by transfection experiments. Results: The RNA levels of the HCCs were significantly higher than those of the nontumor liver tissues and normal livers (P < 0.001). GEP protein staining was observed in tumor cytoplasm, and the GEP protein levels of the HCCs were also significantly higher than those of the nontumor liver tissues and normal livers (P < 0.001). The majority of HCCs demonstrated up-regulation of GEP protein compared with their adjacent liver tissues [79 (71.8%) of 110]. Positive correlation of GEP RNA with protein levels was observed in HCCs (P < 0.01). Strong GEP expression was associated with large HCCs, venous infiltration, and early intrahepatic recurrence (P < 0.05). Functional studies on the HCC cell line Hep3B demonstrated that reduction of GEP protein levels resulted in decreased cell proliferation rates, tumor invasion ability, anchorage-independent growth in soft agar, and tumorigenicity in nude mice (P < 0.05). Conclusion: GEP is an important factor for HCC growth, invasion, and metastasis. GEP has the potential to serve as a tumor marker and therapeutic target.
Persistent Identifierhttp://hdl.handle.net/10722/148697
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, STen_HK
dc.contributor.authorWong, SYen_HK
dc.contributor.authorLeung, KLen_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorSo, Sen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2012-05-29T06:14:45Z-
dc.date.available2012-05-29T06:14:45Z-
dc.date.issued2004en_HK
dc.identifier.citationClinical Cancer Research, 2004, v. 10 n. 22, p. 7629-7636en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148697-
dc.description.abstractPurpose: Granulin-epithelin precursor (GEP) is a novel growih factor. Our earlier cDNA microarray study indicated that GEP was overexpressed in hepatocellular carcinoma (HCC). The aim of this study was to investigate the clinical significance of GEP expression and its potential as a therapeutic target in HCC. Experimental Design: A total of 110 pairs of HCCs and adjacent nontumor liver tissues, and 22 normal liver tissues were examined. The GEP RNA level was examined by quantitative reverse transcription-PCR, and protein localization by immunohistochemistry. The GEP function was examined by transfection experiments. Results: The RNA levels of the HCCs were significantly higher than those of the nontumor liver tissues and normal livers (P < 0.001). GEP protein staining was observed in tumor cytoplasm, and the GEP protein levels of the HCCs were also significantly higher than those of the nontumor liver tissues and normal livers (P < 0.001). The majority of HCCs demonstrated up-regulation of GEP protein compared with their adjacent liver tissues [79 (71.8%) of 110]. Positive correlation of GEP RNA with protein levels was observed in HCCs (P < 0.01). Strong GEP expression was associated with large HCCs, venous infiltration, and early intrahepatic recurrence (P < 0.05). Functional studies on the HCC cell line Hep3B demonstrated that reduction of GEP protein levels resulted in decreased cell proliferation rates, tumor invasion ability, anchorage-independent growth in soft agar, and tumorigenicity in nude mice (P < 0.05). Conclusion: GEP is an important factor for HCC growth, invasion, and metastasis. GEP has the potential to serve as a tumor marker and therapeutic target.en_HK
dc.languageengen_US
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshCarcinoma, Hepatocellular - Metabolism - Pathologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshDna, Complementary - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIntercellular Signaling Peptides And Proteins - Biosynthesisen_US
dc.subject.meshLiver - Metabolismen_US
dc.subject.meshLiver Neoplasms - Metabolism - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshNeoplasm Metastasisen_US
dc.subject.meshNeoplasm Transplantationen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshRna - Metabolismen_US
dc.subject.meshRecurrenceen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTransfectionen_US
dc.subject.meshUp-Regulationen_US
dc.titleGranulin-epithelin precursor overexpression promotes growth and invasion of hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ST: stcheung@hkucc.hku.hken_HK
dc.identifier.emailWong, SY: ashley@pathology.hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hk-
dc.identifier.authorityCheung, ST=rp00457en_HK
dc.identifier.authorityNg, IO=rp00335en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1158/1078-0432.CCR-04-0960en_HK
dc.identifier.pmid15569995-
dc.identifier.scopuseid_2-s2.0-9344229795en_HK
dc.identifier.hkuros96575-
dc.identifier.hkuros139526-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9344229795&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue22en_HK
dc.identifier.spage7629en_HK
dc.identifier.epage7636en_HK
dc.identifier.isiWOS:000225351400023-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, ST=7202473497en_HK
dc.identifier.scopusauthoridWong, SY=7404590342en_HK
dc.identifier.scopusauthoridLeung, KL=7401860603en_HK
dc.identifier.scopusauthoridChen, X=8978110800en_HK
dc.identifier.scopusauthoridSo, S=7102397384en_HK
dc.identifier.scopusauthoridNg, IO=7102753722en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.customcontrol.immutablesml 130703-

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