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Article: Inhibition of hepatocellular carcinoma invasion by suppression of claudin-10 in HLE cells

TitleInhibition of hepatocellular carcinoma invasion by suppression of claudin-10 in HLE cells
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://mct.aacrjournals.org/
Citation
Molecular Cancer Therapeutics, 2007, v. 6 n. 11, p. 2858-2867 How to Cite?
AbstractPreviously, we showed that down-regulation of claudin-10 (CLDN-10) in hepatocellular carcinoma is associated with prolonged disease-free survival after curative surgery. Claudins are important tight junction components. Increasing evidence shows that claudins are involved in cancer progression but each member of claudins is specifically expressed in a variety of malignancies. The biological role of CLDN-10 in hepatocellular carcinoma is unexplored. In the current study, we investigated the CLDN-10 function in two different hepatocellular carcinoma cell lines by in vitro assays with the CLDN-10 overexpression and small interfering RNA-mediated knockdown transfectants. We observed that overexpression of CLDN-10 conferred malignant phenotypes to hepatocellular carcinoma cells, Hep3B, which lack CLDN-10 expression, by promoting cancer cell survival, motility, and invasiveness. More importantly, matrix metalloproteinase 2 (MMP2) was up-regulated. Increase in mRNA transcription and protein expression of membrane type 1-MMP (MT1-MMP) was also observed in the CLDN-10 transfectants, where MT1-MMP was a protease shown to promote intrahepatic metastasis in hepatocellular carcinoma in our earlier study. In addition, CLDN-1, CLDN-2, and CLDN-4 was up-regulated in CLDN-10 overexpression transfectants, indicating that the expression of CLDN-10 in cancer cells might affect the expression levels of its family members. On the contrary, small interfering RNA - based knockdown of CLDN-10 in HLE, an invasive cell line with high level of CLDN-10 expression, abolished invasion and strongly decreased activation of MMPs and claudin members expression. These findings showed that CLDN-10 is functionally involved in hepatocellular carcinoma invasion and is a potential target for hepatocellular carcinoma therapy. Copyright © 2007 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/83989
ISSN
2015 Impact Factor: 5.579
2015 SCImago Journal Rankings: 3.224
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorIp, YCen_HK
dc.contributor.authorCheung, STen_HK
dc.contributor.authorLee, YTen_HK
dc.contributor.authorHo, JCen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:47:36Z-
dc.date.available2010-09-06T08:47:36Z-
dc.date.issued2007en_HK
dc.identifier.citationMolecular Cancer Therapeutics, 2007, v. 6 n. 11, p. 2858-2867en_HK
dc.identifier.issn1535-7163en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83989-
dc.description.abstractPreviously, we showed that down-regulation of claudin-10 (CLDN-10) in hepatocellular carcinoma is associated with prolonged disease-free survival after curative surgery. Claudins are important tight junction components. Increasing evidence shows that claudins are involved in cancer progression but each member of claudins is specifically expressed in a variety of malignancies. The biological role of CLDN-10 in hepatocellular carcinoma is unexplored. In the current study, we investigated the CLDN-10 function in two different hepatocellular carcinoma cell lines by in vitro assays with the CLDN-10 overexpression and small interfering RNA-mediated knockdown transfectants. We observed that overexpression of CLDN-10 conferred malignant phenotypes to hepatocellular carcinoma cells, Hep3B, which lack CLDN-10 expression, by promoting cancer cell survival, motility, and invasiveness. More importantly, matrix metalloproteinase 2 (MMP2) was up-regulated. Increase in mRNA transcription and protein expression of membrane type 1-MMP (MT1-MMP) was also observed in the CLDN-10 transfectants, where MT1-MMP was a protease shown to promote intrahepatic metastasis in hepatocellular carcinoma in our earlier study. In addition, CLDN-1, CLDN-2, and CLDN-4 was up-regulated in CLDN-10 overexpression transfectants, indicating that the expression of CLDN-10 in cancer cells might affect the expression levels of its family members. On the contrary, small interfering RNA - based knockdown of CLDN-10 in HLE, an invasive cell line with high level of CLDN-10 expression, abolished invasion and strongly decreased activation of MMPs and claudin members expression. These findings showed that CLDN-10 is functionally involved in hepatocellular carcinoma invasion and is a potential target for hepatocellular carcinoma therapy. Copyright © 2007 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://mct.aacrjournals.org/en_HK
dc.relation.ispartofMolecular Cancer Therapeuticsen_HK
dc.titleInhibition of hepatocellular carcinoma invasion by suppression of claudin-10 in HLE cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1535-7163&volume=6&issue=11&spage=2858&epage=67&date=2007&atitle=Inhibition+of+hepatocellular+carcinoma+invasion+by+suppression+of+claudin-10+in+HLE+cellsen_HK
dc.identifier.emailSiu, TC: stcheung@hkucc.hku.hken_HK
dc.identifier.authoritySiu, TC=rp00457en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1535-7163.MCT-07-0453en_HK
dc.identifier.pmid18025272en_HK
dc.identifier.scopuseid_2-s2.0-36749050385en_HK
dc.identifier.hkuros139537en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-36749050385&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2858en_HK
dc.identifier.epage2867en_HK
dc.identifier.isiWOS:000251096600004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYing, CI=14039827000en_HK
dc.identifier.scopusauthoridSiu, TC=7202473497en_HK
dc.identifier.scopusauthoridYuk, TL=14632582400en_HK
dc.identifier.scopusauthoridHo, JC=7402650173en_HK
dc.identifier.scopusauthoridSheung, TF=6506234707en_HK

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