RUNX3 is multifunctional in carcinogenesis of multiple solid tumors

被引:122
作者
Chuang, L. S. H. [2 ]
Ito, Y. [1 ,2 ,3 ]
机构
[1] Natl Univ Singapore, Inst Mol & Cell Biol, Canc Sci Inst, Singapore 138673, Singapore
[2] Natl Univ Singapore, Canc Biol Program, Canc Sci Inst Singapore, Singapore 138673, Singapore
[3] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore 138673, Singapore
基金
新加坡国家研究基金会;
关键词
RUNX3; tumor suppressor; solid tumors; functional inactivation; TGF-beta; Wnt; ONCOGENE-INDUCED SENESCENCE; PIM-1 KINASE PHOSPHORYLATES; FOXO TRANSCRIPTION FACTORS; GASTRIC EPITHELIAL-CELLS; PROMOTER HYPERMETHYLATION; GENE-EXPRESSION; PROTEIN MISLOCALIZATION; CONFERS RESISTANCE; INSERTION LOCUS; DOWN-REGULATION;
D O I
10.1038/onc.2010.88
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
The study of RUNX3 in tumor pathogenesis is a rapidly expanding area of cancer research. Functional inactivation of RUNX3-through mutation, epigenetic silencing, or cytoplasmic mislocalization-is frequently observed in solid tumors of diverse origins. This alone indicates that RUNX3 inactivation is a major risk factor in tumorigenesis and that it occurs early during progression to malignancy. Conversely, RUNX3 has also been described to have an oncogenic function in a subset of tumors. Although the mechanism of how RUNX3 switches from tumor suppressive to oncogenic activity is unclear, this is of clinical relevance with implications for cancer detection and prognosis. Recent developments have significantly contributed to our understanding of the pleiotropic tumor suppressive properties of RUNX3 that regulate major signaling pathways. This review summarizes the important findings that link RUNX3 to tumor suppression. Oncogene (2010) 29, 2605-2615; doi:10.1038/onc.2010.88; published online 29 March 2010
引用
收藏
页码:2605 / 2615
页数:11
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