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PU.1调节淋巴瘤细胞中正向调节结构域I结合因子1/Blimp-1的转录。

PU.1 regulates positive regulatory domain I-binding factor 1/Blimp-1 transcription in lymphoma cells.

作者信息

Desai Shruti, Bolick Sophia C E, Maurin Michelle, Wright Kenneth L

机构信息

H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.

出版信息

J Immunol. 2009 Nov 1;183(9):5778-87. doi: 10.4049/jimmunol.0901120. Epub 2009 Oct 14.

Abstract

The human positive regulatory domain I-binding factor 1 (PRDI-BF1) and its murine homolog Blimp-1 promote differentiation of mature B cells into Ab-secreting plasma cells. In contrast, ectopic expression of PRDI-BF1 in lymphoma cells can lead to inhibition of proliferation or apoptosis. However, little is currently known about the regulation of PRDM1, the gene encoding PRDI-BF1. This report establishes that in lymphoma cells stimulation through the BCR rapidly induces endogenous PRDM1 at the level of transcription with minor changes in mRNA stability. The induced PRDM1-encoded protein localizes to its target genes in vivo and suppresses their expression. In vivo genomic footprinting of the PRDM1 promoter in unstimulated lymphoma and myeloma cells reveals multiple common in vivo occupied elements throughout the promoter. Further functional and structural analysis of the promoter reveals that the promoter is preloaded and poised for activation in the B cell lines. The transcription factor PU.1 is shown to be required for the BCR-induced expression of PRDM1 in lymphoma cells and in PU.1-positive myeloma cells. Activation of PRDM1 is associated with loss of the corepressor transducin-like enhancer of split 4 from the PU.1 complex. These findings indicate that PRDM1 is poised for activation in lymphoma cells and therefore may be a potential therapeutic target to inhibit lymphoma cell proliferation and survival.

摘要

人类正调控域I结合因子1(PRDI-BF1)及其小鼠同源物Blimp-1可促进成熟B细胞分化为分泌抗体的浆细胞。相反,PRDI-BF1在淋巴瘤细胞中的异位表达可导致增殖抑制或凋亡。然而,目前对于编码PRDI-BF1的基因PRDM1的调控了解甚少。本报告证实,在淋巴瘤细胞中,通过BCR刺激可在转录水平迅速诱导内源性PRDM1,而mRNA稳定性仅有微小变化。诱导产生的PRDM1编码蛋白在体内定位于其靶基因并抑制其表达。在未受刺激的淋巴瘤和骨髓瘤细胞中对PRDM1启动子进行体内基因组足迹分析,发现在整个启动子区域有多个常见的体内占据元件。对该启动子进行进一步的功能和结构分析表明,该启动子在B细胞系中预先加载并准备好被激活。转录因子PU.1被证明是淋巴瘤细胞和PU.1阳性骨髓瘤细胞中BCR诱导PRDM1表达所必需的。PRDM1的激活与共抑制因子分裂样增强子转导蛋白样4从PU.1复合物中丢失有关。这些发现表明,PRDM1在淋巴瘤细胞中已准备好被激活,因此可能是抑制淋巴瘤细胞增殖和存活的潜在治疗靶点。

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