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Article: Cyclooxygenase-2 pathway correlates with vascular endothelial growth factor expression and tumor angiogenesis in hepatitis B virus-associated hepatocellular carcinoma.

TitleCyclooxygenase-2 pathway correlates with vascular endothelial growth factor expression and tumor angiogenesis in hepatitis B virus-associated hepatocellular carcinoma.
Authors
Issue Date2004
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/
Citation
International Journal Of Oncology, 2004, v. 24 n. 4, p. 853-860 How to Cite?
AbstractEvidence indicates that cyclooxygenase (COX)-2-derived prostaglandins (PGs) contribute to tumor growth by inducing angiogenesis. We investigated the role of COX-2 in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). COX-2 and vascular endothelial growth factor (VEGF) expressions were examined by immunohistochemistry in 24 HBV-associated HCC. Tumor micro-vessel density (MVD) was assessed using CD34 immunohistochemistry. Hep3B HCC cell line, which carries integrated HBV genome, was stably transfected with human COX-2 cDNA. COX-2 and VEGF expressions were determined by Western blot while PG level was determined by ELISA. The effects of PGs on VEGF expression were also investigated. Expression of COX-2 and VEGF in HCC cells were observed in 19 (79%) and 16 (67%) cases, respectively. Well-differentiated HCC expressed COX-2 more strongly than less-differentiated HCC (p<0.001). COX-2 expression was found to correlate with VEGF expression and MVD (p=0.003 and 0.004, respectively). COX-2 overexpressing Hep3B clone had higher VEGF expression as compared to non-COX-2 expressing clone and parental cells. Treatment of the COX-2 overexpressing cells with a COX-2-selective inhibitor, NS-398 (10 microM), decreased PGE2 level and attenuated VEGF expression. Addition of PGE2 (10 microM) and the stable analog of PGI2, carbaprostacyclin (5 microM), to Hep3B cells also increased VEGF expression. Up-regulation of COX-2 correlates with VEGF expression and tumor angiogenesis in HBV-associated HCC. Moreover, COX-2 up-regulates VEGF expression in HCC cells, possibly via PGs production. Selective inhibition of COX-2 may block HCC associated angiogenesis and thus provides a rational approach for treatment of this malignancy.
Persistent Identifierhttp://hdl.handle.net/10722/162836
ISSN
2015 Impact Factor: 3.018
2015 SCImago Journal Rankings: 1.270
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheng, ASen_US
dc.contributor.authorChan, HLen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorLeung, WKen_US
dc.contributor.authorChan, KKen_US
dc.contributor.authorLiew, CTen_US
dc.contributor.authorSung, JJen_US
dc.date.accessioned2012-09-05T05:24:06Z-
dc.date.available2012-09-05T05:24:06Z-
dc.date.issued2004en_US
dc.identifier.citationInternational Journal Of Oncology, 2004, v. 24 n. 4, p. 853-860en_US
dc.identifier.issn1019-6439en_US
dc.identifier.urihttp://hdl.handle.net/10722/162836-
dc.description.abstractEvidence indicates that cyclooxygenase (COX)-2-derived prostaglandins (PGs) contribute to tumor growth by inducing angiogenesis. We investigated the role of COX-2 in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). COX-2 and vascular endothelial growth factor (VEGF) expressions were examined by immunohistochemistry in 24 HBV-associated HCC. Tumor micro-vessel density (MVD) was assessed using CD34 immunohistochemistry. Hep3B HCC cell line, which carries integrated HBV genome, was stably transfected with human COX-2 cDNA. COX-2 and VEGF expressions were determined by Western blot while PG level was determined by ELISA. The effects of PGs on VEGF expression were also investigated. Expression of COX-2 and VEGF in HCC cells were observed in 19 (79%) and 16 (67%) cases, respectively. Well-differentiated HCC expressed COX-2 more strongly than less-differentiated HCC (p<0.001). COX-2 expression was found to correlate with VEGF expression and MVD (p=0.003 and 0.004, respectively). COX-2 overexpressing Hep3B clone had higher VEGF expression as compared to non-COX-2 expressing clone and parental cells. Treatment of the COX-2 overexpressing cells with a COX-2-selective inhibitor, NS-398 (10 microM), decreased PGE2 level and attenuated VEGF expression. Addition of PGE2 (10 microM) and the stable analog of PGI2, carbaprostacyclin (5 microM), to Hep3B cells also increased VEGF expression. Up-regulation of COX-2 correlates with VEGF expression and tumor angiogenesis in HBV-associated HCC. Moreover, COX-2 up-regulates VEGF expression in HCC cells, possibly via PGs production. Selective inhibition of COX-2 may block HCC associated angiogenesis and thus provides a rational approach for treatment of this malignancy.en_US
dc.languageengen_US
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/en_US
dc.relation.ispartofInternational journal of oncologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCarcinoma, Hepatocellular - Blood Supply - Enzymology - Virologyen_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshDinoprostone - Metabolismen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHepatitis B - Virologyen_US
dc.subject.meshHepatitis B Virus - Isolation & Purificationen_US
dc.subject.meshHumansen_US
dc.subject.meshIsoenzymes - Metabolismen_US
dc.subject.meshLiver Neoplasms - Blood Supply - Enzymology - Virologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNeovascularization, Pathologic - Pathologyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshUp-Regulationen_US
dc.subject.meshVascular Endothelial Growth Factors - Metabolismen_US
dc.titleCyclooxygenase-2 pathway correlates with vascular endothelial growth factor expression and tumor angiogenesis in hepatitis B virus-associated hepatocellular carcinoma.en_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid15010822-
dc.identifier.scopuseid_2-s2.0-1842852639en_US
dc.identifier.volume24en_US
dc.identifier.issue4en_US
dc.identifier.spage853en_US
dc.identifier.epage860en_US
dc.identifier.isiWOS:000220412600012-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridCheng, AS=7402075036en_US
dc.identifier.scopusauthoridChan, HL=16038785900en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridChan, KK=8599737700en_US
dc.identifier.scopusauthoridLiew, CT=35809476000en_US
dc.identifier.scopusauthoridSung, JJ=35405352400en_US

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