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IRF4 和 NF-κB 驱动的成人 T 细胞白血病/淋巴瘤中的前馈调节环。

Feed-forward regulatory loop driven by IRF4 and NF-κB in adult T-cell leukemia/lymphoma.

机构信息

Cancer Science Institute of Singapore, National University of Singapore, Singapore.

Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.

出版信息

Blood. 2020 Mar 19;135(12):934-947. doi: 10.1182/blood.2019002639.

Abstract

Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive hematological malignancy derived from mature CD4+ T-lymphocytes. Here, we demonstrate the transcriptional regulatory network driven by 2 oncogenic transcription factors, IRF4 and NF-κB, in ATL cells. Gene expression profiling of primary ATL samples demonstrated that the IRF4 gene was more highly expressed in ATL cells than in normal T cells. Chromatin immunoprecipitation sequencing analysis revealed that IRF4-bound regions were more frequently found in super-enhancers than in typical enhancers. NF-κB was found to co-occupy IRF4-bound regulatory elements and formed a coherent feed-forward loop to coordinately regulate genes involved in T-cell functions and development. Importantly, IRF4 and NF-κB regulated several cancer genes associated with super-enhancers in ATL cells, including MYC, CCR4, and BIRC3. Genetic inhibition of BIRC3 induced growth inhibition in ATL cells, implicating its role as a critical effector molecule downstream of the IRF4-NF-κB transcriptional network.

摘要

成人 T 细胞白血病/淋巴瘤(ATL)是一种源自成熟 CD4+ T 淋巴细胞的高度侵袭性血液恶性肿瘤。在这里,我们展示了由 2 个致癌转录因子 IRF4 和 NF-κB 驱动的 ATL 细胞中的转录调控网络。对原发性 ATL 样本的基因表达谱分析表明,IRF4 基因在 ATL 细胞中的表达水平高于正常 T 细胞。染色质免疫沉淀测序分析显示,IRF4 结合区域在超增强子中比在典型增强子中更常见。发现 NF-κB 与 IRF4 结合的调节元件共同占据,并形成一个连贯的前馈环,共同调节参与 T 细胞功能和发育的基因。重要的是,IRF4 和 NF-κB 在 ATL 细胞中调节了几个与超增强子相关的癌症基因,包括 MYC、CCR4 和 BIRC3。BIRC3 的遗传抑制诱导 ATL 细胞生长抑制,暗示其作为 IRF4-NF-κB 转录网络下游的关键效应分子的作用。

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