National Cancer Institute, National Institutes of Health, Bethesda, MD.
National Cancer Institute, National Institutes of Health, Bethesda, MD.
Semin Oncol. 2017 Dec;44(6):377-380. doi: 10.1053/j.seminoncol.2018.01.004. Epub 2018 Apr 12.
Since 2003, the US Food and Drug Administration approval of bortezomib, a proteasome inhibitor, has changed the management of hematologic malignancies and dramatically improved outcomes for patients with multiple myeloma and mantle cell lymphoma. Since that time, two additional proteasome inhibitors (carfilzomib and ixazomib) have been approved, with other agents and combinations currently under investigation. Proteasomes degrade ubiquitinated proteins or substrates through the ubiquitin-proteasome pathway, a pathway that is utilized in multiple myeloma because of the high protein turnover with immunoglobulin production. Proteasome inhibitors exploit dependence on this pathway, halting protein degradation that ultimately results in apoptosis and cell death. Here we will discuss the structure of the proteasome and the mechanisms of action for proteasome inhibitors to further understand their role in hematologic malignancies.
自 2003 年以来,蛋白酶体抑制剂硼替佐米获得美国食品药品监督管理局批准,改变了血液系统恶性肿瘤的治疗方法,显著改善了多发性骨髓瘤和套细胞淋巴瘤患者的预后。此后,又有两种蛋白酶体抑制剂(卡非佐米和伊沙佐米)获得批准,其他药物和联合用药目前正在研究中。蛋白酶体通过泛素蛋白酶体途径降解泛素化蛋白或底物,由于免疫球蛋白生成导致蛋白质周转率高,多发性骨髓瘤中利用了该途径。蛋白酶体抑制剂利用对该途径的依赖性,阻止蛋白降解,最终导致细胞凋亡和死亡。本文将讨论蛋白酶体的结构和蛋白酶体抑制剂的作用机制,以进一步了解它们在血液系统恶性肿瘤中的作用。