Kasprzyk Marta Elżbieta, Sura Weronika, Podralska Marta, Kazimierska Marta, Seitz Annika, Łosiewski Wojciech, Woźniak Tomasz, Guikema Jeroen E J, Diepstra Arjan, Kluiver Joost, Van den Berg Anke, Rozwadowska Natalia, Dzikiewicz-Krawczyk Agnieszka
Institute of Human Genetics, Polish Academy of Sciences, Poznań.
Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen.
Haematologica. 2024 Dec 1;109(12):4007-4020. doi: 10.3324/haematol.2023.284672.
Chromosomal translocations in non-Hodgkin lymphoma (NHL) result in activation of oncogenes by placing them under the regulation of immunoglobulin heavy chain (IGH) super-enhancers. Aberrant expression of translocated oncogenes induced by enhancer activity can contribute to lymphomagenesis. The role of the IGH enhancers in normal B-cell development is well established, but knowledge regarding the precise mechanisms of their involvement in control of the translocated oncogenes is limited. The goal of this project was to define the critical regions in the IGH regulatory elements and identify enhancer RNA (eRNA). We designed a single guide RNA library densely covering the IGH enhancers and performed tiling CRISPR interference screens in three NHL cell lines. This revealed three regions crucial for NHL cell growth. With chromatin- enriched RNA sequencing we showed transcription from the core enhancer regions and subsequently validated expression of the eRNA in a panel of NHL cell lines and tissue samples. Inhibition of the essential IGH enhancer regions decreased expression of eRNA and translocated oncogenes in several NHL cell lines. The observed expression and growth patterns were consistent with the breakpoints in the IGH locus. Moreover, targeting the Eμ enhancer resulted in loss of B-cell receptor expression. In a Burkitt lymphoma cell line, MYC overexpression partially rescued the phenotype induced by IGH enhancer inhibition. Our results indicated the most critical regions in the IGH enhancers and provided new insights into the current understanding of the role of IGH enhancers in B-cell NHL. As such, this study forms a basis for development of potential therapeutic approaches.
非霍奇金淋巴瘤(NHL)中的染色体易位通过将癌基因置于免疫球蛋白重链(IGH)超级增强子的调控之下,导致癌基因激活。增强子活性诱导的易位癌基因异常表达可促进淋巴瘤的发生。IGH增强子在正常B细胞发育中的作用已得到充分证实,但关于其参与调控易位癌基因的确切机制的了解有限。本项目的目标是确定IGH调控元件中的关键区域并鉴定增强子RNA(eRNA)。我们设计了一个密集覆盖IGH增强子的单向导RNA文库,并在三种NHL细胞系中进行了平铺式CRISPR干扰筛选。这揭示了对NHL细胞生长至关重要的三个区域。通过染色质富集RNA测序,我们显示了核心增强子区域的转录,并随后在一组NHL细胞系和组织样本中验证了eRNA的表达。抑制必需的IGH增强子区域可降低几种NHL细胞系中eRNA和易位癌基因的表达。观察到的表达和生长模式与IGH基因座中的断点一致。此外,靶向Eμ增强子导致B细胞受体表达丧失。在伯基特淋巴瘤细胞系中,MYC过表达部分挽救了IGH增强子抑制诱导的表型。我们的结果表明了IGH增强子中最关键的区域,并为目前对IGH增强子在B细胞NHL中的作用的理解提供了新的见解。因此,本研究为潜在治疗方法的开发奠定了基础。