Function and mechanism by which interferon regulatory factor-1 inhibits oncogenesis (Review)

被引:45
作者
Chen, Fei-Fei [1 ]
Jiang, Guan [1 ]
Xu, Kerui [2 ]
Zheng, Jun-Nian [1 ]
机构
[1] Xuzhou Med Coll, Lab Biol Canc Therapy, Xuzhou 221002, Jiangsu, Peoples R China
[2] Wake Forest Univ, Dept Biol, Salem, NC 27106 USA
关键词
IRF-1; oncogenesis; cell cycle; apoptosis; immune response; TRANSCRIPTION FACTOR IRF-1; VIRUS-MEDIATED TRANSFORMATION; HUMAN B-LYMPHOCYTES; BREAST-CANCER; INDUCED APOPTOSIS; DNA-DAMAGE; SIGNALING PATHWAY; TUMOR SUPPRESSION; CARCINOMA-CELLS; GENE-EXPRESSION;
D O I
10.3892/ol.2012.1051
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
The present review focuses on recent advances in the understanding of the molecular mechnisms by which interferon regulatory factor (IRF)-1 inhibits oncogenesis. IRF-1 is associated with regulation of interferon alpha and beta transcription. In addition, numerous clinical studies have indicated that IRF-1 gene deletion or rearrangement correlates with development of specific forms of human cancer. IRF-1 has been revealed to exhibit marked functional diversity in the regulation of oncogenesis. IRF-1 activates a set of target genes associated with regulation of the cell cycle, apoptosis and the immune response. The role of IRF-1 in the regulation of various types of human tumor has important implications for understanding the susceptibility and progression of cancer. In addition, an improved understanding of the role of IRF-1 in the pathological processes that lead to human malignant diseases may aid development of novel therapeutic strategies.
引用
收藏
页码:417 / 423
页数:7
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