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Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer

Authors
 Seung Won Kim  ;  Ki Cheong Park  ;  Jae Hee Cheon  ;  Won Ho Kim  ;  Tae Il Kim  ;  Tak Bum Ohn  ;  Soung Min Jeon 
Citation
 Cellular Oncology, Vol.36(2) : 169-178, 2013 
Journal Title
 Cellular Oncology 
ISSN
 2211-3428 
Issue Date
2013
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.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/86504
DOI
10.1007/s13402-013-0124-x
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실)
Yonsei Authors
김승원(Kim, Seung Won) ; 김원호(Kim, Won Ho) ; 김태일(Kim, Tae Il) ; 전승민(Jeon, Soung Min) ; 천재희(Cheon, Jae Hee)
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Full Text
http://link.springer.com/article/10.1007%2Fs13402-013-0124-x
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