Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan.
Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Bioorg Med Chem. 2022 Aug 1;67:116764. doi: 10.1016/j.bmc.2022.116764. Epub 2022 May 9.
It is known that p53 is an important transcription factor and plays a central role in ionizing radiation (IR)-induced DNA damage responses such as cell cycle arrest, DNA repair and apoptosis. We previously reported that regulating p53 protein is an effective strategy for modulating cell fate by reducing the acute side effects of radiation therapy. Herein, we report on the discovery of STK160830 as a new radioprotector from a chemical library at The University of Tokyo and the design, synthesis and biological evaluation of its derivatives. The radioprotective activity of STK160830 itself and its derivatives that were synthesized in this work was evaluated using a leukemia cell line, MOLT-4 cells as a model of normal cells that express the p53 protein in a structure-activity relationships (SAR) study. The experimental results suggest that a direct relationship exists between the inhibitory effect of these STK160830 derivatives on the expression level of p53 and their radioprotective activity and that the suppression of p53 by STK160830 derivatives contribute to protecting MOLT-4 cells from apoptosis that is induced by exposure to radiation.
已知 p53 是一种重要的转录因子,在电离辐射(IR)诱导的 DNA 损伤反应中发挥核心作用,如细胞周期阻滞、DNA 修复和细胞凋亡。我们之前曾报道过,通过降低放射治疗的急性副作用来调节 p53 蛋白是调节细胞命运的有效策略。在此,我们报道了从东京大学的化学文库中发现 STK160830 作为一种新型的放射保护剂,并对其衍生物进行了设计、合成和生物学评价。在这项工作中合成的 STK160830 本身及其衍生物的放射保护活性通过白血病细胞系 MOLT-4 细胞作为模型正常细胞进行了评估,这些正常细胞以结构活性关系(SAR)研究的方式表达 p53 蛋白。实验结果表明,这些 STK160830 衍生物对 p53 表达水平的抑制作用与其放射保护活性之间存在直接关系,STK160830 衍生物对 p53 的抑制作用有助于保护 MOLT-4 细胞免受辐射诱导的细胞凋亡。