Kaiser Rainer W J, Erber Johanna, Höpker Katja, Fabretti Francesca, Müller Roman-Ulrich
Medizinische Klinik und Poliklinik I, University Hospital Ludwig-Maximilian-University Munich, Munich, Germany.
Department II of Internal Medicine and Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
Front Oncol. 2020 Jun 10;10:919. doi: 10.3389/fonc.2020.00919. eCollection 2020.
The DNA damage response (DDR) is a complex signaling network that is activated upon genotoxic stress. It determines cellular fate by either activating cell cycle arrest or initiating apoptosis and thereby ensures genomic stability. The Apoptosis Antagonizing Transcription Factor (AATF/Che-1), an RNA polymerase II-interacting transcription factor and known downstream target of major DDR kinases, affects DDR signaling by inhibiting p53-mediated transcription of pro-apoptotic genes and promoting cell cycle arrest through various pathways instead. Specifically, AATF was shown to inhibit p53 expression at the transcriptional level and repress its pro-apoptotic activity by direct binding to p53 protein and transactivation of anti-apoptotic genes. Solid and hematological tumors of various organs exploit this function by overexpressing AATF. Both copy number gains and high expression levels of AATF were associated with worse prognosis or relapse of malignant tumors. Recently, a number of studies have enabled insights into the molecular mechanisms by which AATF affects both DDR and proliferation. AATF was found to directly localize to sites of DNA damage upon laser ablation and interact with DNA repair proteins. In addition, depletion of AATF resulted in increased DNA damage and decrease of both proliferative activity and genotoxic tolerance. Interestingly, considering the role of ribosomal stress in the regulation of p53, more recent work established AATF as ribosomal RNA binding protein and enabled insights into its role as an important factor for rRNA processing and ribosome biogenesis. This Mini Review summarizes recent findings on AATF and its important role in the DDR, malignancy, and ribosome biogenesis.
DNA损伤反应(DDR)是一个复杂的信号网络,在基因毒性应激时被激活。它通过激活细胞周期停滞或启动细胞凋亡来决定细胞命运,从而确保基因组稳定性。凋亡拮抗转录因子(AATF/Che-1)是一种与RNA聚合酶II相互作用的转录因子,也是主要DDR激酶的已知下游靶点,它通过抑制p53介导的促凋亡基因转录来影响DDR信号传导,而是通过各种途径促进细胞周期停滞。具体而言,AATF已被证明在转录水平上抑制p53表达,并通过直接结合p53蛋白和反式激活抗凋亡基因来抑制其促凋亡活性。各种器官的实体瘤和血液肿瘤通过过度表达AATF来利用这一功能。AATF的拷贝数增加和高表达水平都与恶性肿瘤的预后较差或复发有关。最近,一些研究使人们深入了解了AATF影响DDR和增殖的分子机制。发现AATF在激光消融后直接定位于DNA损伤部位,并与DNA修复蛋白相互作用。此外,AATF的缺失导致DNA损伤增加,增殖活性和基因毒性耐受性降低。有趣的是,考虑到核糖体应激在p53调节中的作用,最近的研究将AATF确立为核糖体RNA结合蛋白,并使人们深入了解了其作为rRNA加工和核糖体生物发生重要因子的作用。本综述总结了关于AATF及其在DDR、恶性肿瘤和核糖体生物发生中的重要作用的最新发现。