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首页> 外文期刊>Cell cycle >Bridging the gaps: from risk loci via non-coding RNAs to gene networks and prostate cancer phenotypes.
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Bridging the gaps: from risk loci via non-coding RNAs to gene networks and prostate cancer phenotypes.

机译：缩小差距：从通过非编码RNA的风险位点到基因网络和前列腺癌表型。

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摘要

Defining the functional role for single nucleotide polymorphisms (SNPs) associated with cancer predisposition is an important step in translating genome-wide association studies in the development of surrogate biomarkers and targeted therapies. That the majority of risk-predicting SNPs are intergenic poses significant challenges. SNPs in intergenic regions are thought to confer many of their effects by modulating gene expression. A classical explanation for these effects is that high-risk and low-risk variants either mark changes in transcription factor binding or chromatin architecture elsewhere within the risk locus or actually form part of transcription factor binding sites. SNP-dependent changes in transcription factor occupancy may be critical for modulating the expression of genes located proximally, distally or perhaps even on other chromosomes. Loci of interest can be defined on this basis by chromatin immunoprecipitation and direct sequencing for histone marks characteristic of regions of open/active chromatin and transcription factors, such as the androgen receptor in prostate cancer.
机译：定义与癌症易感性相关的单核苷酸多态性（SNP）的功能作用是在替代生物标志物和靶向疗法的开发中翻译全基因组关联研究的重要步骤。大多数可预测风险的SNP是基因间的，这构成了重大挑战。基因间区域中的SNP被认为通过调节基因表达而赋予其许多作用。对于这些影响的经典解释是，高风险和低风险的变体或者标记了风险位点内其他地方的转录因子结合或染色质结构的变化，或者实际上形成了转录因子结合位点的一部分。 SNP依赖性转录因子占用的变化对于调节位于近端，远端甚至其他染色体上的基因的表达可能至关重要。可以在此基础上通过染色质免疫沉淀和直接测序确定开放/活性染色质和转录因子（例如前列腺癌中的雄激素受体）区域特征的组蛋白标记来定义目标基因座。

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