Upregulation and secretion of kallikrein-related peptidase 6 (KLK6) in gastric cancer

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dc.contributor.authorJ J Kim-
dc.contributor.authorJong-Tae Kim-
dc.contributor.authorH R Yoon-
dc.contributor.authorMin Ah Kang-
dc.contributor.authorJ H Kim-
dc.contributor.authorY H Lee-
dc.contributor.authorJae Wha Kim-
dc.contributor.authorSeon-Jin Lee-
dc.contributor.authorEun Young Song-
dc.contributor.authorP K Myung-
dc.contributor.authorHee Gu Lee-
dc.date.accessioned2017-04-19T09:29:57Z-
dc.date.available2017-04-19T09:29:57Z-
dc.date.issued2012-
dc.identifier.issn10104283-
dc.identifier.uri10.1007/s13277-011-0267-1ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/10706-
dc.description.abstractKLK6 encoding kallikrein-related peptidase 6, a trypsin-like serine protease, has been shown to be upregulated in several cancers, although the tumorigenic role of KLK6 has not been elucidated. In this study, KLK6 was identified as a highly upregulated gene in gastric cancer; therefore, the possibility that KLK6 might be a suitable candidate tumor marker was examined. RT-PCR and immunohistochemical analysis showed overexpression of KLK6 in gastric cancer tissues compared to nontumor regions. Sera from gastric cancer patients had a 1.7-fold increase in KLK6 (373.1 μg/L, P=0.048) compared to healthy individuals (214.2 μg/L), although there was no significant difference among patients with various tumor stages. Cellular invasiveness decreased by 45% in cells transfected with KLK6-specific small interfering RNA. Exogenous overexpression of KLK6 led to decreased activity of the E-cadherin promoter. This study shows that KLK6 is significantly upregulated and secreted in gastric cancer tissues and sera, suggesting that KLK6 might be used as a potential biomarker and therapeutic target for gastric cancer.-
dc.publisherSpringer Verlag (Germany)ko
dc.titleUpregulation and secretion of kallikrein-related peptidase 6 (KLK6) in gastric cancer-
dc.title.alternativeUpregulation and secretion of kallikrein-related peptidase 6 (KLK6) in gastric cancer-
dc.typeArticle-
dc.citation.titleTumor Biology-
dc.citation.number3-
dc.citation.endPage738-
dc.citation.startPage731-
dc.citation.volume33-
dc.contributor.affiliatedAuthorJong-Tae Kim-
dc.contributor.affiliatedAuthorJae Wha Kim-
dc.contributor.affiliatedAuthorSeon-Jin Lee-
dc.contributor.affiliatedAuthorHee Gu Lee-
dc.contributor.alternativeName김진주-
dc.contributor.alternativeName김종태-
dc.contributor.alternativeName윤효란-
dc.contributor.alternativeName강민아-
dc.contributor.alternativeName김주헌-
dc.contributor.alternativeName이영하-
dc.contributor.alternativeName김재화-
dc.contributor.alternativeName이선진-
dc.contributor.alternativeName송은영-
dc.contributor.alternativeName명평근-
dc.contributor.alternativeName이희구-
dc.identifier.bibliographicCitationTumor Biology, vol. 33, no. 3, pp. 731-738-
dc.identifier.doi10.1007/s13277-011-0267-1-
dc.subject.keywordGastric cancer-
dc.subject.keywordImmunohistochemistry-
dc.subject.keywordInvasiveness-
dc.subject.keywordKallikrein-
dc.subject.keywordKLK6-
dc.subject.localGastric cancer-
dc.subject.localImmunohistochemistry-
dc.subject.localInvasiveness-
dc.subject.localKallikrein-
dc.subject.localKLK6-
dc.description.journalClassN-
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Division of Biomaterials Research > Cell Factory Research Center > 1. Journal Articles
Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
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