Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-04

AUTHORS

Seung Won Kim, Ki Cheong Park, Soung Min Jeon, Tak Bum Ohn, Tae Il Kim, Won Ho Kim, Jae Hee Cheon

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. More... »

PAGES

169-178

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s13402-013-0124-x

DOI

http://dx.doi.org/10.1007/s13402-013-0124-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1029677681

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23378274


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