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Article: Twist overexpression correlates with hepatocellular carcinoma metastasis through induction of epithelial-mesenchymal transition

TitleTwist overexpression correlates with hepatocellular carcinoma metastasis through induction of epithelial-mesenchymal transition
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2006, v. 12 n. 18, p. 5369-5376 How to Cite?
AbstractPurpose: Hepatocellular carcinoma (HCC) is a rapidly growing tumor associated with a high propensity for vascular invasion and metastasis. Epithelial-mesenchymal transition (EMT) is a key event in the tumor invasion process. Recently, Twist has been identified to play an important role in EMT-mediated metastasis through the regulation of E-cadherin expression. However, the actual role of Twist in tumor invasiveness remains unclear. The purpose of this study is to investigate the expression and possible role of Twist in HCC. Experimental Design: We evaluated Twist and E-cadherin expression in HCC tissue microarray of paired primary and metastatic HCC by immunohistochemical staining. The role of Twist in EMT-mediated invasiveness was also evaluated in vitro in HCC cell lines. Results: We first showed that overexpression of Twist was correlated with HCC metastasis (P = 0.001) and its expression was negatively correlated with E-cadherin expression (P = 0.001, r = -0.443) by tissue microarray. A significant increase of Twist at the mRNA level was also found in metastatic HCC cell lines MHCC-97H, MHCC-97L, and H2M when compared with nonmetastatic Huh-7, H2P, and PLC cell lines. The MHCC-97H cell line, which has a higher metastatic ability, was found to have a higher level of Twist than MHCC-97L. Accompanied with increased Twist expression in the metastatic HCC cell lines when compared with the nonmetastatic primary ones, we found decreased E-cadherin mRNA expression in the metastatic HCC cell lines. By ectopic transfection of Twist into PLC cells, Twist was able to suppress E-cadherin expression and induce EMT changes, which was correlated with increased HCC cell invasiveness. Conclusion: This study shows that Twist overexpression was correlated with HCC metastasis through induction of EMT changes and HCC cell invasiveness. © 2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/67692
ISSN
2021 Impact Factor: 13.801
2020 SCImago Journal Rankings: 5.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, TKen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorYuen, APen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorKwok, WKen_HK
dc.contributor.authorWang, XHen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorChau, KLen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T05:57:24Z-
dc.date.available2010-09-06T05:57:24Z-
dc.date.issued2006en_HK
dc.identifier.citationClinical Cancer Research, 2006, v. 12 n. 18, p. 5369-5376en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67692-
dc.description.abstractPurpose: Hepatocellular carcinoma (HCC) is a rapidly growing tumor associated with a high propensity for vascular invasion and metastasis. Epithelial-mesenchymal transition (EMT) is a key event in the tumor invasion process. Recently, Twist has been identified to play an important role in EMT-mediated metastasis through the regulation of E-cadherin expression. However, the actual role of Twist in tumor invasiveness remains unclear. The purpose of this study is to investigate the expression and possible role of Twist in HCC. Experimental Design: We evaluated Twist and E-cadherin expression in HCC tissue microarray of paired primary and metastatic HCC by immunohistochemical staining. The role of Twist in EMT-mediated invasiveness was also evaluated in vitro in HCC cell lines. Results: We first showed that overexpression of Twist was correlated with HCC metastasis (P = 0.001) and its expression was negatively correlated with E-cadherin expression (P = 0.001, r = -0.443) by tissue microarray. A significant increase of Twist at the mRNA level was also found in metastatic HCC cell lines MHCC-97H, MHCC-97L, and H2M when compared with nonmetastatic Huh-7, H2P, and PLC cell lines. The MHCC-97H cell line, which has a higher metastatic ability, was found to have a higher level of Twist than MHCC-97L. Accompanied with increased Twist expression in the metastatic HCC cell lines when compared with the nonmetastatic primary ones, we found decreased E-cadherin mRNA expression in the metastatic HCC cell lines. By ectopic transfection of Twist into PLC cells, Twist was able to suppress E-cadherin expression and induce EMT changes, which was correlated with increased HCC cell invasiveness. Conclusion: This study shows that Twist overexpression was correlated with HCC metastasis through induction of EMT changes and HCC cell invasiveness. © 2006 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshCadherins - metabolismen_HK
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathology - secondaryen_HK
dc.subject.meshCell Transformation, Neoplastic - metabolismen_HK
dc.subject.meshEpithelial Cells - metabolism - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMicroarray Analysis - methodsen_HK
dc.subject.meshNeoplasm Invasiveness - geneticsen_HK
dc.subject.meshNuclear Proteins - metabolismen_HK
dc.subject.meshStatistics as Topicen_HK
dc.subject.meshTranscriptional Activation - physiologyen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTwist Transcription Factor - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleTwist overexpression correlates with hepatocellular carcinoma metastasis through induction of epithelial-mesenchymal transitionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=12&issue=18&spage=5369&epage=5376&date=2006&atitle=Twist+overexpression+correlates+with+hepatocellular+carcinoma+metastasis+through+induction+of+epithelial-mesenchymal+transitionen_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailLing, MT: patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hken_HK
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityGuan, X=rp00454en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-05-2722en_HK
dc.identifier.pmid17000670-
dc.identifier.scopuseid_2-s2.0-33749344520en_HK
dc.identifier.hkuros124177en_HK
dc.identifier.hkuros137544-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33749344520&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue18en_HK
dc.identifier.spage5369en_HK
dc.identifier.epage5376en_HK
dc.identifier.isiWOS:000240714400019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridYuen, AP=7006290111en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridKwok, WK=14825201200en_HK
dc.identifier.scopusauthoridWang, XH=7501854829en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridGuan, X=7201463221en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridChau, KL=49761149000en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.issnl1078-0432-

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