Reduced Levels of miR-34a in Neuroblastoma Are Not Caused by Mutations in the TP53 Binding Site
Reduced Levels of miR-34a in Neuroblastoma Are Not Caused by Mutations in the TP53 Binding Site
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DOI：
10.1002/gcc.20662
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发表时间：
2009-07-01
影响因子：
3.7
通讯作者：
Yaniv, Isaac
中科院分区：
文献类型：
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作者：
Feinberg-Gorenshtein, Galina;Avigad, Smadar;Yaniv, Isaac
神经母细胞瘤（NB）是5岁以下儿童最常见的颅外实体瘤。miR-34 a位于染色体I带p36，最近被认为是NB中的肿瘤抑制基因。此外，研究表明，miR-34 a通过结合成熟miR-34 a上游的TP 53结合位点而被TP 53激活。我们研究了来自57名患者的NB肿瘤的miR-34 a表达水平、IP状态、TP 53编码区的突变和TP 53结合位点的突变。在携带I p36.3丢失的肿瘤中鉴定到miR-34 a的表达水平降低（P = 0.028）。在TP 53的编码区或TP 53结合位点中未发现突变。因此，结合位点的突变不是NB中miR-34 a失活的额外机制。控制miR-34 a表达的其他调控机制及其与TP 53的关系应进一步探讨。(C)2009 Wiley-Liss，Inc.
Neuroblastoma (NB) is the most common extracranial solid tumor in children below the age of 5 years. miR-34a, located in chromosome band I p36, has been recently implicated as a tumor suppressor gene in NB. In addition, it has been shown that miR-34a is activated by TP53 by binding to a TP53 binding site upstream to the mature miR-34a. We studied NB tumors from 57 patients for miR-34a expression levels, I p status, mutations in the TP53 coding region and mutations of the TP53 binding site. Reduced expression levels of miR-34a were identified in tumors harboring I p36.3 Loss (P = 0.028). No mutations were identified in the coding region of TP53, or in the TP53 binding site. Thus, mutations in the binding site are not an additional mechanism for the inactivation of miR-34a in NB. Other regulatory mechanisms controlling miR-34a expression and its relationship to TP53 should be further explored. (C) 2009 Wiley-Liss, Inc.