Ghelli Luserna Di Rorà Andrea, Iacobucci Ilaria, Imbrogno Enrica, Papayannidis Cristina, Derenzini Enrico, Ferrari Anna, Guadagnuolo Viviana, Robustelli Valentina, Parisi Sarah, Sartor Chiara, Abbenante Maria Chiara, Paolini Stefania, Martinelli Giovanni
Institute of Hematology "L. e A. Seragnoli", Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Bologna, Italy.
Oncotarget. 2016 Aug 16;7(33):53377-53391. doi: 10.18632/oncotarget.10535.
During the last few years many Checkpoint kinase 1/2 (Chk1/Chk2) inhibitors have been developed for the treatment of different type of cancers. In this study we evaluated the efficacy of the Chk 1/2 inhibitor prexasertib mesylate monohydrate in B-/T- cell progenitor acute lymphoblastic leukemia (ALL) as single agent and in combination with other drugs. The prexasertib reduced the cell viability in a dose and time dependent manner in all the treated cell lines. The cytotoxic activity was confirmed by the increment of apoptotic cells (Annexin V/Propidium Iodide staining), by the increase of γH2A.X protein expression and by the activation of different apoptotic markers (Parp-1 and pro-Caspase3 cleavage). Furthermore, the inhibition of Chk1 changed the cell cycle profile. In order to evaluate the chemo-sensitizer activity of the compound, different cell lines were treated for 24 and 48 hours with prexasertib in combination with other drugs (imatinib, dasatinib and clofarabine). The results from cell line models were strengthened in primary leukemic blasts isolated from peripheral blood of adult acute lymphoblastic leukemia patients. In this study we highlighted the mechanism of action and the effectiveness of prexasertib as single agent or in combination with other conventional drugs like imatinib, dasatinib and clofarabine in the treatment of B-/T-ALL.
在过去几年中,已研发出多种检查点激酶1/2(Chk1/Chk2)抑制剂用于治疗不同类型的癌症。在本研究中,我们评估了Chk 1/2抑制剂甲磺酸普瑞西替尼一水合物作为单一药物以及与其他药物联合使用时,对B/T细胞祖细胞急性淋巴细胞白血病(ALL)的疗效。普瑞西替尼在所有处理的细胞系中均以剂量和时间依赖性方式降低细胞活力。细胞毒性活性通过凋亡细胞增加(膜联蛋白V/碘化丙啶染色)、γH2A.X蛋白表达增加以及不同凋亡标志物(聚ADP核糖聚合酶-1和前半胱天冬酶3裂解)的激活得到证实。此外,Chk1的抑制改变了细胞周期分布。为了评估该化合物的化学增敏活性,用普瑞西替尼与其他药物(伊马替尼、达沙替尼和氯法拉滨)联合处理不同细胞系24小时和48小时。从成人急性淋巴细胞白血病患者外周血分离的原发性白血病细胞中得到细胞系模型结果的验证。在本研究中,我们突出了普瑞西替尼作为单一药物或与伊马替尼、达沙替尼和氯法拉滨等其他传统药物联合使用时,在治疗B/T-ALL中的作用机制和有效性。