Hess Jessica D, Macias Luca H, Gutierrez Denisse A, Moran-Santibanez Karla, Contreras Lisett, Medina Stephanie, Villanueva Paulina J, Kirken Robert A, Varela-Ramirez Armando, Penichet Manuel L, Aguilera Renato J
Department of Biological Sciences and Cellular Characterization and Biorepository Core Facility, Border Biomedical Research Center, The University of Texas at El Paso (UTEP), El Paso, TX 79902, USA.
Division of Surgical Oncology, Department of Surgery and Department of Microbiology, Immunology and Molecular Genetics, The Molecular Biology Institute, AIDS Institute, Jonsson Comprehensive Cancer Center, The University of California, Los Angeles, CA 90095, USA.
Biology (Basel). 2022 Jun 18;11(6):930. doi: 10.3390/biology11060930.
In recent years, the thienopyrazole moiety has emerged as a pharmacologically active scaffold with antitumoral and kinase inhibitory activity. In this study, high-throughput screening of 2000 small molecules obtained from the ChemBridge DIVERset library revealed a unique thieno[2,3-c]pyrazole derivative (Tpz-1) with potent and selective cytotoxic effects on cancer cells. Compound Tpz-1 consistently induced cell death at low micromolar concentrations (0.19 μM to 2.99 μM) against a panel of 17 human cancer cell lines after 24 h, 48 h, or 72 h of exposure. Furthermore, an in vitro investigation of Tpz-1's mechanism of action revealed that Tpz-1 interfered with cell cycle progression, reduced phosphorylation of p38, CREB, Akt, and STAT3 kinases, induced hyperphosphorylation of Fgr, Hck, and ERK 1/2 kinases, and disrupted microtubules and mitotic spindle formation. These findings support the continued exploration of Tpz-1 and other thieno[2,3-c]pyrazole-based compounds as potential small-molecule anticancer agents.
近年来,噻吩并吡唑部分已成为一种具有抗肿瘤和激酶抑制活性的药理活性支架。在本研究中,对从ChemBridge DIVERset文库获得的2000个小分子进行高通量筛选,发现了一种独特的噻吩并[2,3-c]吡唑衍生物(Tpz-1),对癌细胞具有强效且选择性的细胞毒性作用。化合物Tpz-1在暴露24小时、48小时或72小时后,以低微摩尔浓度(0.19 μM至2.99 μM)对一组17种人类癌细胞系持续诱导细胞死亡。此外,对Tpz-1作用机制的体外研究表明,Tpz-1干扰细胞周期进程,降低p38、CREB、Akt和STAT3激酶的磷酸化水平,诱导Fgr、Hck和ERK 1/2激酶的过度磷酸化,并破坏微管和有丝分裂纺锤体的形成。这些发现支持继续探索Tpz-1和其他基于噻吩并[2,3-c]吡唑的化合物作为潜在的小分子抗癌药物。