Department of Physiology and Biophysics, University of Washington, Health Sciences Building G424, 1705 NE Pacific Str., Seattle, WA, 98195-7280, USA.
Department of Pharmacology, University of Washington, Health Sciences Center F404A, 1959 NE Pacific Str., Seattle, WA, 98195-7280, USA.
J Transl Med. 2024 May 10;22(1):441. doi: 10.1186/s12967-024-05234-3.
Microtubule targeting agents (MTAs) are commonly prescribed to treat cancers and predominantly kill cancer cells in mitosis. Significantly, some MTA-treated cancer cells escape death in mitosis, exit mitosis and become malignant polyploid giant cancer cells (PGCC). Considering the low number of cancer cells undergoing mitosis in tumor tissues, killing them in interphase may represent a favored antitumor approach. We discovered that ST-401, a mild inhibitor of microtubule (MT) assembly, preferentially kills cancer cells in interphase as opposed to mitosis, a cell death mechanism that avoids the development of PGCC. Single cell RNA sequencing identified mRNA transcripts regulated by ST-401, including mRNAs involved in ribosome and mitochondrial functions. Accordingly, ST-401 induces a transient integrated stress response, reduces energy metabolism, and promotes mitochondria fission. This cell response may underly death in interphase and avoid the development of PGCC. Considering that ST-401 is a brain-penetrant MTA, we validated these results in glioblastoma cell lines and found that ST-401 also reduces energy metabolism and promotes mitochondria fission in GBM sensitive lines. Thus, brain-penetrant mild inhibitors of MT assembly, such as ST-401, that induce death in interphase through a previously unanticipated antitumor mechanism represent a potentially transformative new class of therapeutics for the treatment of GBM.
微管靶向剂 (MTA) 常用于治疗癌症,并主要在有丝分裂期杀死癌细胞。值得注意的是,一些经 MTA 处理的癌细胞在有丝分裂期逃脱死亡,退出有丝分裂并成为恶性多倍体巨癌细胞 (PGCC)。考虑到肿瘤组织中经历有丝分裂的癌细胞数量较少,在间期中杀死它们可能代表一种有利的抗肿瘤方法。我们发现 ST-401 是一种微管 (MT) 组装的轻度抑制剂,它优先在间期中杀死癌细胞,而不是在有丝分裂期杀死癌细胞,这种细胞死亡机制避免了 PGCC 的发展。单细胞 RNA 测序鉴定了受 ST-401 调节的 mRNA 转录本,包括参与核糖体和线粒体功能的 mRNA。因此,ST-401 诱导短暂的整合应激反应,降低能量代谢,并促进线粒体分裂。这种细胞反应可能是间期中细胞死亡的基础,并避免 PGCC 的发展。考虑到 ST-401 是一种穿透血脑屏障的 MTA,我们在神经胶质瘤细胞系中验证了这些结果,并发现 ST-401 还降低了能量代谢并促进了 GBM 敏感系中线粒体的分裂。因此,穿透血脑屏障的微管组装轻度抑制剂,如 ST-401,通过以前未预料到的抗肿瘤机制在间期中诱导细胞死亡,代表了治疗 GBM 的一类潜在变革性新治疗方法。