Department of Pathology and Laboratory Medicine and Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Tongji Medical College, School of Pharmacy, Huazhong University of Science and Technology, Room 402, 13 Hangkong Road, Wuhan, Hubei, 430030, People's Republic of China.
Int J Hematol. 2011 Aug;94(2):118-125. doi: 10.1007/s12185-011-0899-3. Epub 2011 Aug 5.
NOTCH1 plays a central role in T-cell development and, when aberrantly activated, in acute T-cell lymphoblastic leukemia (T-ALL). As a transmembrane receptor that is ultimately converted into a transcription factor, NOTCH1 directly activates a spectrum of target genes, which function to mediate NOTCH1 signaling in normal or transformed T cells. During physiologic T-cell development, NOTCH1 has important functions in cell fate determination, proliferation, survival and metabolism. Activating NOTCH1 mutations occur in more than half of human patients with T-ALL, suggesting an important role for aberrant NOTCH1 signaling in the pathogenesis of this disease. Inhibiting NOTCH1 signaling in patient-derived cell lines and murine T-ALLs leads to growth arrest and/or apoptosis suggesting that NOTCH1 inhibitors can improve T-ALL treatment. However, there are challenges to translate NOTCH1 inhibitors to the clinic because of toxicity and resistance. This review focuses on molecular mechanisms of oncogenic NOTCH1 signaling, molecular and functional analysis of NOTCH1 transcriptional targets in T-ALL, and recent advances in therapeutic targeting of NOTCH1.
NOTCH1 在 T 细胞发育中发挥核心作用,在异常激活时,在急性 T 细胞淋巴母细胞白血病(T-ALL)中发挥作用。作为一种最终转化为转录因子的跨膜受体,NOTCH1 直接激活一系列靶基因,这些基因在正常或转化的 T 细胞中发挥介导 NOTCH1 信号的作用。在生理 T 细胞发育过程中,NOTCH1 在细胞命运决定、增殖、存活和代谢中具有重要功能。在超过一半的人类 T-ALL 患者中存在激活 NOTCH1 的突变,这表明异常 NOTCH1 信号在这种疾病的发病机制中起着重要作用。在患者来源的细胞系和鼠 T-ALL 中抑制 NOTCH1 信号会导致生长停滞和/或细胞凋亡,这表明 NOTCH1 抑制剂可以改善 T-ALL 的治疗效果。然而,由于毒性和耐药性,将 NOTCH1 抑制剂转化为临床应用仍存在挑战。本文重点介绍致癌 NOTCH1 信号的分子机制、T-ALL 中 NOTCH1 转录靶标的分子和功能分析,以及 NOTCH1 靶向治疗的最新进展。