Fibroblast growth factor receptor 1 oncogene partner as a novel prognostic biomarker and therapeutic target for lung cancer

被引:33
|
作者
Mano, Yuria
Takahashi, Koji
Ishikawa, Nobuhisa
Takano, Atsushi
Yasui, Wataru
Inai, Kouki
Nishimura, Hitoshi
Tsuchiya, Eiju
Nakamura, Yusuke
Daigo, Yataro
机构
[1] Univ Tokyo, Ctr Human Genome, Inst Med Sci, Mol Med Lab,Minato Ku, Tokyo 1088639, Japan
[2] Hiroshima Univ, Grad Sch Biomed Sci, Dept Mol Pathol, Hiroshima 7348551, Japan
[3] Hiroshima Univ, Grad Sch Biomed Sci, Dept Pathol, Hiroshima 7348551, Japan
[4] Saitama Canc Ctr, Dept Thorac Surg, Saitama 3620806, Japan
[5] Kanagawa Canc Ctr, Res Inst, Asahi Ku, Yokohama, Kanagawa 2410815, Japan
来源
CANCER SCIENCE | 2007年 / 98卷 / 12期
关键词
D O I
10.1111/j.1349-7006.2007.00610.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
To screen candidate molecules that might be useful as diagnostic biomarkers or for development of novel molecular-targeting therapies, we previously carried out gene-expression profile analysis of 101 lung carcinomas and detected an elevated expression of FGFR1OP (fibroblast growth factor receptor 1 oncogene partner) in the majority of lung cancers. Immunohistochemical staining using tumor tissue microarrays consisting of 372 archived non-small cell lung cancer (NSCLC) specimens revealed positive staining of FGFR1OP in 334 (89.8%) of 372 NSCLCs. We also found that the high level of FGFR1OP expression was significantly associated with shorter tumor-specific survival times (P < 0.0001 by log-rank test). Moreover, multivariate analysis determined that FGFR1OP was an independent prognostic factor for surgically treated NSCLC patients (P < 0.0001). Treatment of lung cancer cells, in which endogenous FGFR1OP was overexpressed, using FGFR1OP siRNA, suppressed its expression and resulted in inhibition of the cell growth. Furthermore, induction of FGFR1OP increased the cellular motility and growth-promoting activity of mammalian cells. To investigate its function, we searched for FGFR1OP-interacting proteins in lung cancer cells and identified ABL1 (Abelson murine leukemia viral oncogene homolog 1) and WRNIP1 (Werner helicase interacting protein 1), which was known to be involved in cell cycle progression. FGFR1OP significantly reduced ABL1-dependent phosphorylation of WRNIP1 and resulted in the promotion of cell cycle progression. Because our data imply that FGFR1OP is likely to play a significant role in lung cancer growth and progression, FGFR1OP should be useful as a prognostic biomarker and probably as a therapeutic target for lung cancer.
引用
收藏
页码:1902 / 1913
页数:12
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