Chromosome 1 open reading frame 10 (C1orf10) gene is frequently down-regulated and inhibits cell proliferation in oral squamous cell carcinoma

被引:32
作者
Imai, FL
Uzawa, K
Nimura, Y
Moriya, T
Imai, MA
Shiiba, M
Bukawa, H
Yokoe, H
Tanzawa, H
机构
[1] Chiba Univ, Grad Sch Med, Dept Clin Mol Biol, Chuo Ku, Chiba 2608670, Japan
[2] Chiba Univ, Grad Sch Sci & Technol, Inage Ku, Chiba 2638522, Japan
[3] Chiba Univ, Grad Sch Med, Dept Funct Genom, Chuo Ku, Chiba 2608670, Japan
[4] Chiba Univ Hosp, Div Oral Surg, Chuo Ku, Chiba 2608670, Japan
[5] Chiba Univ, Grad Sch Med, Ctr Excellence Program Century 21, Chuo Ku, Chiba 2608670, Japan
关键词
C1orf10; oral squamous cell carcinoma (OSCC); cell proliferation; down-regulation; transfection;
D O I
10.1016/j.biocel.2005.02.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chromosome 1 open reading frame 10 (C1orf10) is a recently identified gene encoding a protein with an 5100 EF-hand calcium-binding motif, and its expression is known to be down-regulated in esophageal squamous cell carcinoma. In this study, to determine whether the loss of C1orf10 gene function could contribute to the development of oral squamous cell carcinoma (OSCC), we have evaluated the expression status of this gene by reverse transcriptase-polymerise chain reaction (RT-PCR) analysis and quantitative real-time PCR analysis. A high frequency of decrease in C1 orf10 gene was detected not only in OSCC-derived cell lines but also in tumor tissues. Next, to define biological function of this gene in oral carcinogenesis, we transfected C1orf10 with an Ecdysone-inducible system in OSCC cell lines and analyzed the effects of its overexpression. Induction of C1orf10 expression resulted in a significant decline in the rate of cell proliferation, and in an arrest in the G, phase of the cell cycle, with a down-regulation of Cyclin D1 expression. However, we could not detect significant difference in the percentage of apoptotic cells. Thus, our results suggest that the down-regulation of C1 orf10 gene plays a role in oral carcinogenesis, and that its expression may negatively regulate OSCC cell proliferation by arresting the cell cycle. (C) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1641 / 1655
页数:15
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