Understanding the role of miRNA in regulating NF-κB in blood cancer

被引:0
|
作者
Rushworth, Stuart A. [1 ]
Murray, Megan Y. [1 ]
Barrera, Lawrence N. [1 ]
Heasman, Sally-Anne [1 ]
Zaitseva, Lyubov [1 ]
MacEwan, David J. [1 ]
机构
[1] Univ E Anglia, Sch Pharm, Norwich NR4 7TJ, Norfolk, England
来源
AMERICAN JOURNAL OF CANCER RESEARCH | 2012年 / 2卷 / 01期
关键词
Leukemia; NF-kappa B; microRNA; gene regulation; apoptosis; ACUTE MYELOID-LEUKEMIA; TUMOR-NECROSIS-FACTOR; DOWN-REGULATION; THERAPEUTIC TARGET; MICRORNA; ACTIVATION; APOPTOSIS; PROTEIN; GENES; TRANSCRIPTION;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by binding to complementary sequences in mRNAs encoding downstream target genes. A large variety of cellular processes, including differentiation, development, apoptosis and cell cycle progression, are dependent on miRNA-mediated suppression of gene expression for their regulation. As such, it is unsurprising that these small RNA molecules are associated with signaling networks that are often altered in various diseases, including many blood cancers. One such network is the nuclear factor-kappa B (NF-kappa B) pathways that universally stimulate transcription of proteins which generally promote cell survival, inhibit apoptosis, allow cellular growth, induce angiogenesis and generate many pro-inflammatory responses. The NF-kappa B signalling pathway is often constitutively activated in blood cell cancers including myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML), acute lymphocytic leukaemia (ALL), chronic myeloid leukaemia (CML), chronic lymphocytic leukaemia (CLL), lymphomas and in multiple myeloma (MM). This review focuses on the function of miRNAs that directly target NF-kappa B signaling cascade. Recent findings that connect this pathway through various miRNA families to human blood cancers are reviewed, and support for using miRNA-based therapy as a novel method to counteract this tumour-promoting signalling event is discussed.
引用
收藏
页码:65 / 74
页数:10
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