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Syndecan-1, a key regulator of cell viability in endometrial cancer.

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dc.contributor.authorChoi, DS-
dc.contributor.authorKim, JH-
dc.contributor.authorRyu, HS-
dc.contributor.authorKim, HC-
dc.contributor.authorHan, JH-
dc.contributor.authorLee, JS-
dc.contributor.authorMin, CK-
dc.date.accessioned2011-03-07T05:52:37Z-
dc.date.available2011-03-07T05:52:37Z-
dc.date.issued2007-
dc.identifier.issn0020-7136-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/1568-
dc.description.abstractSyndecan-1 is one of the major proteoglycans on cell surfaces involved in major biological processes. Although loss of syndecan-1 correlates well with the gain of cancerous characteristics in a wide range of cancers, increased expression of syndecan-1 also coincides with adverse outcomes in some cancers, including breast, ovarian and pancreatic cancers. For this Janus-faced attitude of syndecan-1, we sought to examine expression patterns of syndecan-1 in endometrial carcinoma (EC) and gain insight into the roles of syndecan-1. Immunohistochemical examinations of 109 endometrial tissue samples from myoma, hyperplasia and EC uteri revealed that syndecan-1 expression was significantly upregulated in EC compared with hyperplasia (p < 0.001). To evaluate pathophysiological functions of syndecan-1, its expression level was altered, and subsequent outcomes were examined using human endometrial cancer cell lines such as HEC-1A, AN3CA and KLE cells. Overexpression of syndecan-1 increased the growth of HEC-1A cells regardless of anchorage dependence while silencing syndecan-1 by antisense RNAs caused apoptotic cell death. Consistent with decreased viability, the loss of syndecan-1 was also accompanied by a decrease in the activation of Erk and Akt and a concomitant decrease in the phosphorylation of PTEN and PDK1, which are known as negative and positive regulators of Akt activation, respectively. These down-regulatory effects were reversed upon overexpression of syndecan-1. Collectively together, the aforementioned findings lend support to the notion that upregulation of syndecan-1 may be a critical element for endometrial cancers in maintaining their viability and thus can serve as a cancer specific therapeutic and diagnostic marker.-
dc.language.isoen-
dc.subject.MESHApoptosis-
dc.subject.MESHCell Line-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Survival-
dc.subject.MESHEndometrial Neoplasms-
dc.subject.MESHEndometrium-
dc.subject.MESHExtracellular Signal-Regulated MAP Kinases-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHPTEN Phosphohydrolase-
dc.subject.MESHPhosphorylation-
dc.subject.MESHProto-Oncogene Proteins c-akt-
dc.subject.MESHRNA Interference-
dc.subject.MESHSignal Transduction-
dc.subject.MESHSyndecan-1-
dc.subject.MESHUp-Regulation-
dc.titleSyndecan-1, a key regulator of cell viability in endometrial cancer.-
dc.typeArticle-
dc.identifier.pmid17455248-
dc.contributor.affiliatedAuthor유, 희석-
dc.contributor.affiliatedAuthor한, 재호-
dc.type.localJournal Papers-
dc.identifier.doi10.1002/ijc.22713-
dc.citation.titleInternational journal of cancer-
dc.citation.volume121-
dc.citation.number4-
dc.citation.date2007-
dc.citation.startPage741-
dc.citation.endPage750-
dc.identifier.bibliographicCitationInternational journal of cancer, 121(4). : 741-750, 2007-
dc.identifier.eissn1097-0215-
dc.relation.journalidJ000207136-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Obstetrics & Gynecology
Journal Papers > School of Medicine / Graduate School of Medicine > Pathology
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