Affar Malik, Bottardi Stefania, Quansah Norreen, Lemarié Maud, Ramón Ailyn C, Affar El Bachir, Milot Eric
Faculty of Medicine, University of Montreal, Montréal, QC, Canada.
Maisonneuve-Rosemont Hospital Research Center, CIUSSS de l'Est-de-l'Île de Montréal, 5415 boulevard de l'Assomption, Montréal, QC, H1T 2M4, Canada.
Cell Death Differ. 2025 Jan;32(1):37-55. doi: 10.1038/s41418-023-01212-2. Epub 2023 Aug 24.
IKAROS is a master regulator of cell fate determination in lymphoid and other hematopoietic cells. This transcription factor orchestrates the association of epigenetic regulators with chromatin, ensuring the expression pattern of target genes in a developmental and lineage-specific manner. Disruption of IKAROS function has been associated with the development of acute lymphocytic leukemia, lymphoma, chronic myeloid leukemia and immune disorders. Paradoxically, while IKAROS has been shown to be a tumor suppressor, it has also been identified as a key therapeutic target in the treatment of various forms of hematological malignancies, including multiple myeloma. Indeed, targeted proteolysis of IKAROS is associated with decreased proliferation and increased death of malignant cells. Although the molecular mechanisms have not been elucidated, the expression levels of IKAROS are variable during hematopoiesis and could therefore be a key determinant in explaining how its absence can have seemingly opposite effects. Mechanistically, IKAROS collaborates with a variety of proteins and complexes controlling chromatin organization at gene regulatory regions, including the Nucleosome Remodeling and Deacetylase complex, and may facilitate transcriptional repression or activation of specific genes. Several transcriptional regulatory functions of IKAROS have been proposed. An emerging mechanism of action involves the ability of IKAROS to promote gene repression or activation through its interaction with the RNA polymerase II machinery, which influences pausing and productive transcription at specific genes. This control appears to be influenced by IKAROS expression levels and isoform production. In here, we summarize the current state of knowledge about the biological roles and mechanisms by which IKAROS regulates gene expression. We highlight the dynamic regulation of this factor by post-translational modifications. Finally, potential avenues to explain how IKAROS destruction may be favorable in the treatment of certain hematological malignancies are also explored.
IKAROS是淋巴细胞和其他造血细胞中细胞命运决定的主要调节因子。这种转录因子协调表观遗传调节因子与染色质的结合,以发育和谱系特异性方式确保靶基因的表达模式。IKAROS功能的破坏与急性淋巴细胞白血病、淋巴瘤、慢性髓性白血病和免疫紊乱的发生有关。矛盾的是,虽然IKAROS已被证明是一种肿瘤抑制因子,但它也被确定为治疗包括多发性骨髓瘤在内的各种血液系统恶性肿瘤的关键治疗靶点。事实上,IKAROS的靶向蛋白水解与恶性细胞增殖减少和死亡增加有关。尽管分子机制尚未阐明,但IKAROS的表达水平在造血过程中是可变的,因此可能是解释其缺失如何产生看似相反效果的关键决定因素。从机制上讲,IKAROS与多种控制基因调控区域染色质组织的蛋白质和复合物协同作用,包括核小体重塑和去乙酰化酶复合物,并可能促进特定基因的转录抑制或激活。IKAROS的几种转录调节功能已被提出。一种新出现的作用机制涉及IKAROS通过与RNA聚合酶II机制相互作用促进基因抑制或激活的能力,这会影响特定基因处的暂停和有效转录。这种控制似乎受IKAROS表达水平和异构体产生的影响。在此,我们总结了关于IKAROS调节基因表达的生物学作用和机制的当前知识状态。我们强调了通过翻译后修饰对该因子的动态调节。最后,还探讨了解释IKAROS破坏在某些血液系统恶性肿瘤治疗中可能有利的潜在途径。