Collagen Triple Helix Repeat Containing 1 (CTHRC1) acts via ERK-dependent induction of MMP9 to promote invasion of colorectal cancer cells

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dc.contributor.authorH C Kim-
dc.contributor.authorYong Sung Kim-
dc.contributor.authorHyun Woo Oh-
dc.contributor.authorK Kim-
dc.contributor.authorS S Oh-
dc.contributor.authorJong-Tae Kim-
dc.contributor.authorBo Yeon Kim-
dc.contributor.authorSeon-Jin Lee-
dc.contributor.authorYong Kyung Choe-
dc.contributor.authorD H Kim-
dc.contributor.authorS H Kim-
dc.contributor.authorS W Chae-
dc.contributor.authorK D Kim-
dc.contributor.authorHee Gu Lee-
dc.date.accessioned2017-04-19T09:51:07Z-
dc.date.available2017-04-19T09:51:07Z-
dc.date.issued2014-
dc.identifier.issn1949-2553-
dc.identifier.uri10.18632/oncotarget.1714ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11843-
dc.description.abstractCollagen triple helix repeat-containing 1 (CTHRC1) is known to be aberrantly upregulated in most human solid tumors, although the functional roles of CTHRC1 in colorectal cancer remain unclear. In this study, we investigated the occurrence of CTHRC1 upregulation and its role in vivo and in vitro. The expression profile and clinical importance of CTHRC1 were examined by reverse transcription-polymerase chain reaction and immunohistochemical analyses in normal and tumor patient samples. CTHRC1 was detectable in normal tissues, but also was highly expressed in tumor specimens. CTHRC1 upregulation was significantly associated with demethylation of the CTHRC1 promoter in colon cancer cell lines and tumor tissues. Clinicopathologic analyses showed that nodal status and expression of CTHRC1 (95% CI 0.999-3.984, p=0.05) were significant prognostic factors for disease-free survival. Promoter CpG methylation and hypermethylation status were measured by bisulfite sequencing and pyrosequencing analysis. Furthermore, we showed that overexpression of CTHRC1 in the SW480 and HT-29 cell lines increased invasiveness, an effect mediated by extracellular signal-regulated kinase (ERK)-dependent upregulation of matrix metalloproteinase 9 (MMP9). Consistent with this, we found that knockdown of CTHRC1 attenuated ERK activation and cancer cell invasivity. These results demonstrate that CTHRC1 expression is elevated in human colon cancer cell lines and clinical specimens, and promotes cancer cell invasivity through ERK-dependent induction of MMP9 expression. Our results further suggest that high levels of CTHRC1 expression are associated with poor clinical outcomes.-
dc.publisherImpact Journalsko
dc.titleCollagen Triple Helix Repeat Containing 1 (CTHRC1) acts via ERK-dependent induction of MMP9 to promote invasion of colorectal cancer cells-
dc.title.alternativeCollagen Triple Helix Repeat Containing 1 (CTHRC1) acts via ERK-dependent induction of MMP9 to promote invasion of colorectal cancer cells-
dc.typeArticle-
dc.citation.titleOncotarget-
dc.citation.number2-
dc.citation.endPage529-
dc.citation.startPage519-
dc.citation.volume5-
dc.contributor.affiliatedAuthorYong Sung Kim-
dc.contributor.affiliatedAuthorHyun Woo Oh-
dc.contributor.affiliatedAuthorJong-Tae Kim-
dc.contributor.affiliatedAuthorBo Yeon Kim-
dc.contributor.affiliatedAuthorSeon-Jin Lee-
dc.contributor.affiliatedAuthorYong Kyung Choe-
dc.contributor.affiliatedAuthorHee Gu Lee-
dc.contributor.alternativeName김희철-
dc.contributor.alternativeName김용성-
dc.contributor.alternativeName오현우-
dc.contributor.alternativeName김권일-
dc.contributor.alternativeName오상석-
dc.contributor.alternativeName김종태-
dc.contributor.alternativeName김보연-
dc.contributor.alternativeName이선진-
dc.contributor.alternativeName최용경-
dc.contributor.alternativeName김동혁-
dc.contributor.alternativeName김석형-
dc.contributor.alternativeName채성완-
dc.contributor.alternativeName김광동-
dc.contributor.alternativeName이희구-
dc.identifier.bibliographicCitationOncotarget, vol. 5, no. 2, pp. 519-529-
dc.identifier.doi10.18632/oncotarget.1714-
dc.description.journalClassN-
Appears in Collections:
Division of Bio Technology Innovation > Core Research Facility & Analysis Center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
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