Department of Pathology, Oslo University Hospital - Norwegian Radium Hospital, Montebello, 0310, Oslo, Norway.
Institute for Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Sci Rep. 2017 Aug 1;7(1):7040. doi: 10.1038/s41598-017-07226-4.
The contribution of mutations in regulatory regions to tumorigenesis has been the subject of many recent studies. We propose a new framework for integrative analysis of genome-wide sequencing data by considering diverse genetic information. This approach is applied to study follicular lymphoma (FL), a disease for which little is known about the contribution of regulatory gene mutations. Results from a test FL cohort revealed three novel highly recurrent regulatory mutation blocks near important genes implicated in FL, BCL6 and BCL2. Similar findings were detected in a validation FL cohort. We also found transcription factors (TF) whose binding may be disturbed by these mutations in FL: disruption of FOX TF family near the BCL6 promoter may result in reduced BCL6 expression, which then increases BCL2 expression over that caused by BCL2 gene translocation. Knockdown experiments of two TF hits (FOXD2 or FOXD3) were performed in human B lymphocytes verifying that they modulate BCL6/BCL2 according to the computationally predicted effects of the SNVs on TF binding. Overall, our proposed integrative analysis facilitates non-coding driver identification and the new findings may enhance the understanding of FL.
调控区域突变在肿瘤发生中的作用一直是许多近期研究的主题。我们提出了一种新的框架,通过考虑多种遗传信息来综合分析全基因组测序数据。该方法应用于研究滤泡性淋巴瘤 (FL),对于调控基因突变在 FL 中的作用,人们知之甚少。对一个测试性 FL 队列的研究结果揭示了三个新的高度复发的调控突变块,这些突变块靠近与 FL 相关的重要基因 BCL6 和 BCL2。在一个验证性的 FL 队列中也发现了类似的发现。我们还发现了转录因子 (TF),这些突变可能会干扰它们在 FL 中的结合:在 BCL6 启动子附近 FOX 家族 TF 的破坏可能导致 BCL6 表达减少,进而增加 BCL2 表达,超过 BCL2 基因易位引起的表达增加。在人 B 淋巴细胞中对两个 TF 命中 (FOXD2 或 FOXD3) 进行了敲低实验,验证了它们根据 SNV 对 TF 结合的计算预测效应来调节 BCL6/BCL2。总的来说,我们提出的综合分析有助于识别非编码驱动基因,新的发现可能会增进对 FL 的理解。