Cited 55 times in
Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer
DC Field | Value | Language |
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dc.contributor.author | 김승원 | - |
dc.contributor.author | 김원호 | - |
dc.contributor.author | 김태일 | - |
dc.contributor.author | 전승민 | - |
dc.contributor.author | 천재희 | - |
dc.contributor.author | 박기청 | - |
dc.date.accessioned | 2014-12-18T08:32:36Z | - |
dc.date.available | 2014-12-18T08:32:36Z | - |
dc.date.issued | 2013 | - |
dc.identifier.issn | 2211-3428 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/86504 | - |
dc.description.abstract | BACKGROUND: Although it has been well established that galectin-4 is selectively expressed by intestinal epithelial cells, the role of galectin-4 in colorectal cancer (CRC) development is, as yet, poorly understood. Here, we aimed to explore the role of galectin-4 in CRC development, both in vitro and in vivo. METHODS: Galectin-4 expression was investigated in tissue specimens from patients with adenoma, carcinoma and ulcerative colitis (UC) using immunohistochemistry. Colorectal cancer-derived HT-29 cells, in which galectin-4 expression was knocked down, were established using shRNA. mRNA and protein expression levels of galectin-4 and several downstream cancer-related genes were analyzed using RT-PCR, qPCR array, Western blotting, and immunofluorescence assays. To investigate the effect of galectin-4 expression abrogation on tumorigenesis in vivo, xenograft assays were performed. RESULTS: Immunohistochemistry analyses showed high expression levels of galectin-4 in normal colon mucosa tissues. Conversely, the expression levels of galectin-4 were significantly lower in CRC samples and its precursor lesions with dysplasia or inflammation. We found that shRNA-mediated galectin-4 silencing increases cell proliferation and, concomitantly, activates NF-κB and STAT3 signaling along with IL-6 up-regulation. In addition, we found that shRNA-mediated galectin-4 silencing promotes the expression of NF-κB target genes and other cancer-related genes and, concomitantly, enhances the in vivo growth of xenografts. CONCLUSIONS: We show that abrogation of galectin-4 expression promotes cancer cell proliferation and, for the first time, provide evidence that down-regulation of galectin-4 elicits tumor promotion in vitro and in vivo through activation of IL-6/NF-κB/STAT3 signaling. | - |
dc.description.statementOfResponsibility | open | - |
dc.relation.isPartOf | CELLULAR ONCOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Yonsei Biomedical Research Center (연세의생명연구원) | - |
dc.contributor.googleauthor | Seung Won Kim | - |
dc.contributor.googleauthor | Ki Cheong Park | - |
dc.contributor.googleauthor | Soung Min Jeon | - |
dc.contributor.googleauthor | Tak Bum Ohn | - |
dc.contributor.googleauthor | Tae Il Kim | - |
dc.contributor.googleauthor | Won Ho Kim | - |
dc.contributor.googleauthor | Jae Hee Cheon | - |
dc.identifier.doi | 10.1007/s13402-013-0124-x | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00774 | - |
dc.contributor.localId | A01079 | - |
dc.contributor.localId | A03526 | - |
dc.contributor.localId | A04030 | - |
dc.contributor.localId | A00656 | - |
dc.relation.journalcode | J00500 | - |
dc.identifier.eissn | 2211-3436 | - |
dc.identifier.pmid | Colorectal cancer ; Galectin-4 ; Interleukin 6 ; NF-κB ; STAT3 | - |
dc.identifier.url | http://link.springer.com/article/10.1007%2Fs13402-013-0124-x | - |
dc.subject.keyword | Colorectal cancer | - |
dc.subject.keyword | Galectin-4 | - |
dc.subject.keyword | Interleukin 6 | - |
dc.subject.keyword | NF-κB | - |
dc.subject.keyword | STAT3 | - |
dc.contributor.alternativeName | Kim, Seung Won | - |
dc.contributor.alternativeName | Kim, Won Ho | - |
dc.contributor.alternativeName | Kim, Tae Il | - |
dc.contributor.alternativeName | Jeon, Soung Min | - |
dc.contributor.alternativeName | Cheon, Jae Hee | - |
dc.contributor.affiliatedAuthor | Kim, Won Ho | - |
dc.contributor.affiliatedAuthor | Kim, Tae Il | - |
dc.contributor.affiliatedAuthor | Jeon, Soung Min | - |
dc.contributor.affiliatedAuthor | Cheon, Jae Hee | - |
dc.contributor.affiliatedAuthor | Kim, Seung Won | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 36 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 169 | - |
dc.citation.endPage | 178 | - |
dc.identifier.bibliographicCitation | CELLULAR ONCOLOGY, Vol.36(2) : 169-178, 2013 | - |
dc.identifier.rimsid | 29021 | - |
dc.type.rims | ART | - |
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