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HuR Knockdown Changes the Oncogenic Potential of Oral Cancer Cells

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/45096

Title: HuR Knockdown Changes the Oncogenic Potential of Oral Cancer Cells
Authors: Kakuguchi, Wataru Browse this author
Kitamura, Tetsuya Browse this author
Kuroshima, Takeshi Browse this author
Ishikawa, Makoto Browse this author
Kitagawa, Yoshimasa Browse this author
Totsuka, Yasunori Browse this author
Shindoh, Masanobu Browse this author
Higashino, Fumihiro Browse this author
Keywords: HuR
knockdown
AU-rich element
anchorage-independent cell growth
cell cycle-related proteins
Issue Date: Apr-2010
Publisher: American Association for Cancer Research
Journal Title: Molecular Cancer Research
Volume: 8
Issue: 4
Start Page: 520
End Page: 528
Publisher DOI: 10.1158/1541-7786.MCR-09-0367
PMID: 20332213
Abstract: HuR binds to AU-rich element (ARE) containing mRNA to protect them from rapid degradation. Here, we show that knockdown of HuR changes the oncogenic properties of oral cancer cells. Oral squamous cell carcinoma cell lines, HSC-3 and Ca9.22, which express HuR protein and cytoplasmic ARE-mRNA more abundantly than normal cells, were subjected to HuR knockdown. In the HuR-knockdown cancer cells, the cytoplasmic expression of c-fos, c-myc, and COX-2 mRNAs was inhibited compared to those in cells that had been transfected with a control siRNA, and the half-lives of these mRNAs were shorter than those of their counterparts in the control cells. HuR-knockdown cells failed to make colonies in soft agar, suggesting that the cells had lost their ability for anchorage-independent cell growth. Additionally, the motile and invasive activities of the cells decreased remarkably by HuR knockdown. Furthermore, the expression of cell cycle-related proteins, such as cyclin A, cyclin B1, cyclin D1, and CDK1, was reduced in the HuR-knockdown cancer cells, and HuR bound to cdk1 mRNA in order to stabilize it. These findings suggest that HuR knockdown changes the features of oral cancer cells, at least in part, by affecting their cell cycle, and shows potential as an effective therapeutic approach.
Type: article (author version)
URI: http://hdl.handle.net/2115/45096
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 東野 史裕

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