Molecular analysis of pediatric brain tumors identifies microRNAs in pilocytic astrocytomas that target the MAPK and NF-κB pathways.
Molecular analysis of pediatric brain tumors identifies microRNAs in pilocytic astrocytomas that target the MAPK and NF-κB pathways.
复制标题
小儿脑肿瘤的分子分析可鉴定靶向MAPK和NF-κB途径的毛囊星形胶质细胞瘤中的microRNA。
DOI:
10.1186/s40478-015-0266-3
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发表时间:
2015-12-18
影响因子:
7.1
通讯作者:
Sheer D
中科院分区:
文献类型:
--
作者:
Jones TA;Jeyapalan JN;Forshew T;Tatevossian RG;Lawson AR;Patel SN;Doctor GT;Mumin MA;Picker SR;Phipps KP;Michalski A;Jacques TS;Sheer D
Pilocytic astrocytomas are slow-growing tumors that usually occur in the cerebellum or in the midline along the hypothalamic/optic pathways. The most common genetic alterations in pilocytic astrocytomas activate the ERK/MAPK signal transduction pathway, which is a major driver of proliferation but is also believed to induce senescence in these tumors. Here, we have conducted a detailed investigation of microRNA and gene expression, together with pathway analysis, to improve our understanding of the regulatory mechanisms in pilocytic astrocytomas. Pilocytic astrocytomas were found to have distinctive microRNA and gene expression profiles compared to normal brain tissue and a selection of other pediatric brain tumors. Several microRNAs found to be up-regulated in pilocytic astrocytomas are predicted to target the ERK/MAPK and NF-κB signaling pathways as well as genes involved in senescence-associated inflammation and cell cycle control. Furthermore, IGFBP7 and CEBPB, which are transcriptional inducers of the senescence-associated secretory phenotype (SASP), were also up-regulated together with the markers of senescence and inflammation, CDKN1A (p21), CDKN2A (p16) and IL1B. These findings provide further evidence of a senescent phenotype in pilocytic astrocytomas. In addition, they suggest that the ERK/MAPK pathway, which is considered the major driver of these tumors, is regulated not only by genetic aberrations but also by microRNAs. The online version of this article (doi:10.1186/s40478-015-0266-3) contains supplementary material, which is available to authorized users.