Bernasconi-Elias P, Hu T, Jenkins D, Firestone B, Gans S, Kurth E, Capodieci P, Deplazes-Lauber J, Petropoulos K, Thiel P, Ponsel D, Hee Choi S, LeMotte P, London A, Goetcshkes M, Nolin E, Jones M D, Slocum K, Kluk M J, Weinstock D M, Christodoulou A, Weinberg O, Jaehrling J, Ettenberg S A, Buckler A, Blacklow S C, Aster J C, Fryer C J
Developmental and Molecular Pathways, Novartis Institutes for Biomedical Research, Cambridge, MA, USA.
Center for Proteomic Chemistry, Novartis Institutes for Biomedical Research, Cambridge, MA, USA.
Oncogene. 2016 Nov 24;35(47):6077-6086. doi: 10.1038/onc.2016.133. Epub 2016 May 9.
Notch receptors have been implicated as oncogenic drivers in several cancers, the most notable example being NOTCH1 in T-cell acute lymphoblastic leukemia (T-ALL). To characterize the role of activated NOTCH3 in cancer, we generated an antibody that detects the neo-epitope created upon gamma-secretase cleavage of NOTCH3 to release its intracellular domain (ICD3), and sequenced the negative regulatory region (NRR) and PEST (proline, glutamate, serine, threonine) domain coding regions of NOTCH3 in a panel of cell lines. We also characterize NOTCH3 tumor-associated mutations that result in activation of signaling and report new inhibitory antibodies. We determined the structural basis for receptor inhibition by obtaining the first co-crystal structure of a NOTCH3 antibody with the NRR protein and defined two distinct epitopes for NRR antibodies. The antibodies exhibit potent anti-leukemic activity in cell lines and tumor xenografts harboring NOTCH3 activating mutations. Screening of primary T-ALL samples reveals that 2 of 40 tumors examined show active NOTCH3 signaling. We also identified evidence of NOTCH3 activation in 12 of 24 patient-derived orthotopic xenograft models, 2 of which exhibit activation of NOTCH3 without activation of NOTCH1. Our studies provide additional insights into NOTCH3 activation and offer a path forward for identification of cancers that are likely to respond to therapy with NOTCH3 selective inhibitory antibodies.
Notch受体在多种癌症中被认为是致癌驱动因子,最显著的例子是T细胞急性淋巴细胞白血病(T-ALL)中的NOTCH1。为了表征活化的NOTCH3在癌症中的作用,我们制备了一种抗体,该抗体可检测NOTCH3经γ-分泌酶切割释放其细胞内结构域(ICD3)时产生的新表位,并对一组细胞系中NOTCH3的负调控区域(NRR)和PEST(脯氨酸、谷氨酸、丝氨酸、苏氨酸)结构域编码区进行了测序。我们还对导致信号激活的NOTCH3肿瘤相关突变进行了表征,并报告了新的抑制性抗体。通过获得NOTCH3抗体与NRR蛋白的首个共晶体结构,我们确定了受体抑制的结构基础,并定义了NRR抗体的两个不同表位。这些抗体在携带NOTCH3激活突变的细胞系和肿瘤异种移植物中表现出强大的抗白血病活性。对原发性T-ALL样本的筛查显示,在检测的40个肿瘤中有2个显示出活跃的NOTCH3信号。我们还在24个患者来源的原位异种移植模型中的12个中发现了NOTCH3激活的证据,其中2个表现出NOTCH3激活而NOTCH1未激活。我们的研究为NOTCH3激活提供了更多见解,并为识别可能对NOTCH3选择性抑制性抗体治疗有反应的癌症提供了一条前进的道路。