NDLI: Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer

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Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer

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Cellular Oncology : Volume 36, Issue 1, February 2013

Cellular Oncology : Volume 35

Cellular Oncology : Volume 34

Abrogation of galectin-4 expression promotes tumorigenesis in colorectal cancer

Content Provider	Springer Nature Link
Author	Kim, Seung Won Park, Ki Cheong Jeon, Soung Min Ohn, Tak Bum Kim, Tae Il Kim, Won Ho Cheon, Jae Hee
Copyright Year	2013
Abstract	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.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.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.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.
Starting Page	169
Ending Page	178
Page Count	10
File Format	PDF
ISSN	22113428
Journal	Cellular Oncology
Volume Number	36
Issue Number	2
e-ISSN	22113436
Language	English
Publisher	Springer Netherlands
Publisher Date	2013-02-02
Publisher Institution	International Society for Cellular Oncology
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Colorectal cancer Galectin-4 Interleukin 6 NF-κB STAT3 Cancer Research Biomedicine general Pathology Oncology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Molecular Medicine Oncology

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