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Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Dental Medicine / Faculty of Dental Medicine >
Peer-reviewed Journal Articles, etc >
HuR Knockdown Changes the Oncogenic Potential of Oral Cancer Cells
| 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)
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Submitter: 東野 史裕
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