Wang Jingnan, Li Jianfeng, Santana-Santos Lucas, Shuda Masahiro, Sobol Robert W, Van Houten Bennett, Qian Wei
Tsinghua University School of Medicine, Tsinghua University, Haidian District, Beijing 100084, China.
Department of Pharmacology & Chemical Biology, University of Pittsburgh School of Medicine and Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213, USA.
Mol Oncol. 2015 Feb;9(2):488-502. doi: 10.1016/j.molonc.2014.10.002. Epub 2014 Oct 17.
Traditional antimitotic drugs for cancer chemotherapy often have undesired toxicities to healthy tissues, limiting their clinical application. Developing novel agents that specifically target tumor cell mitosis is needed to minimize the toxicity and improve the efficacy of this class of anticancer drugs. We discovered that mdivi-1 (mitochondrial division inhibitor-1), which was originally reported as an inhibitor of mitochondrial fission protein Drp1, specifically disrupts M phase cell cycle progression only in human tumor cells, but not in non-transformed fibroblasts or epithelial cells. The antimitotic effect of mdivi-1 is Drp1 independent, as mdivi-1 induces M phase abnormalities in both Drp1 wild-type and Drp1 knockout SV40-immortalized/transformed MEF cells. We also identified that the tumor transformation process required for the antimitotic effect of mdivi-1 is downstream of SV40 large T and small t antigens, but not hTERT-mediated immortalization. Mdivi-1 induces multipolar mitotic spindles in tumor cells regardless of their centrosome numbers. Acentrosomal spindle poles, which do not contain the bona-fide centrosome components γ-tubulin and centrin-2, were found to contribute to the spindle multipolarity induced by mdivi-1. Gene expression profiling revealed that the genes involved in oocyte meiosis and assembly of acentrosomal microtubules are highly expressed in tumor cells. We further identified that tumor cells have enhanced activity in the nucleation and assembly of acentrosomal kinetochore-attaching microtubules. Mdivi-1 inhibited the integration of acentrosomal microtubule-organizing centers into centrosomal asters, resulting in the development of acentrosomal mitotic spindles preferentially in tumor cells. The formation of multipolar acentrosomal spindles leads to gross genome instability and Bax/Bak-dependent apoptosis. Taken together, our studies indicate that inducing multipolar spindles composing of acentrosomal poles in mitosis could achieve tumor-specific antimitotic effect, and mdivi-1 thus represents a novel class of compounds as acentrosomal spindle inducers (ASI).
用于癌症化疗的传统抗有丝分裂药物常常对健康组织产生不良毒性,限制了它们的临床应用。需要开发专门靶向肿瘤细胞有丝分裂的新型药物,以将这类抗癌药物的毒性降至最低并提高疗效。我们发现,mdivi-1(线粒体分裂抑制剂-1)最初被报道为线粒体分裂蛋白Drp1的抑制剂,它仅在人类肿瘤细胞中特异性破坏M期细胞周期进程,而在未转化的成纤维细胞或上皮细胞中则不会。mdivi-1的抗有丝分裂作用不依赖于Drp1,因为mdivi-1在Drp1野生型和Drp1基因敲除的SV40永生化/转化的MEF细胞中均诱导M期异常。我们还确定,mdivi-1抗有丝分裂作用所需的肿瘤转化过程位于SV40大T抗原和小t抗原的下游,但不依赖于hTERT介导的永生化。mdivi-1在肿瘤细胞中诱导多极有丝分裂纺锤体,无论其中心体数量如何。发现不含真正中心体成分γ-微管蛋白和中心蛋白-2的无中心体纺锤体极,促成了mdivi-1诱导的纺锤体多极性。基因表达谱分析显示,参与卵母细胞减数分裂和无中心体微管组装的基因在肿瘤细胞中高度表达。我们进一步确定,肿瘤细胞在无中心体动粒附着微管的成核和组装方面具有增强的活性。mdivi-1抑制无中心体微管组织中心融入中心体星状体,导致无中心体有丝分裂纺锤体优先在肿瘤细胞中形成。多极无中心体纺锤体的形成导致严重的基因组不稳定和Bax/Bak依赖性凋亡。综上所述,我们的研究表明,在有丝分裂中诱导由无中心体极组成的多极纺锤体可以实现肿瘤特异性抗有丝分裂作用,因此mdivi-1代表了一类新型化合物,即无中心体纺锤体诱导剂(ASI)。