a QIMR Berghofer Medical Research Institute , Herston , QLD , Australia.
b University of Queensland Diamantina Institute , The University of Queensland, Translational Research Institute, Brisbane , QLD , Australia.
Cell Cycle. 2019 Jan;18(1):7-15. doi: 10.1080/15384101.2018.1559557. Epub 2019 Jan 2.
Targeting the mitotic machinery using anti-mitotic drugs for elimination of cancer cells is a century-old concept, which continues to be routinely used as a first line of treatment in the clinic. However, patient response remains unpredictable and drug resistance limits effectiveness of these drugs. Cancer cells exit from drug-induced mitotic arrest (mitotic slippage) to avoid subsequent cell death which is thought to be a major mechanism contributing to this resistance. The tumor cells that acquire resistance to anti-mitotic drugs have chromosomal instability (CIN) and are often aneuploid. In this review, we outline the key mechanisms involved in dictating the cell fate during perturbed mitosis and how these processes impede the efficacy of anti-mitotic therapies. Further, we emphasize the recent work from our laboratory, which highlights the functional role of CEP55 in protecting aneuploid cells from death. We also discuss the rationale of targeting CEP55 in vivo, which could prove to be a novel and effective therapeutic strategy for sensitizing cells to microtubule inhibitors and might offer significantly improved patient outcome. Abbreviations: APC/C: Anaphase-Promoting Complex/Cyclosome; BAD: BCL2-Associated agonist of cell Death; BAK1: BCL2 Antagonist Kinase1; BAX: BCL2-Associated X; BCL2: B-cell Chronic Lymphocytic Leukaemia (CLL)/Lymphoma 2; BH: BCL2 Homology Domain; BID: BH3-Interacting domain Death agonist; BIM: BCL2-Interacting Mediator of cell death; BUB: Budding Uninhibited by Benzimidazoles; CDC: Cell Division Cycle; CDH1: Cadherin-1; CDK1: Cyclin-Dependent Kinase 1; CEP55: Centrosomal Protein (55 KDa): CIN: Chromosomal Instability; CTA: Cancer Testis Antigen; EGR1: Early Growth Response protein 1; ERK: Extracellular Signal-Regulated Kinase; ESCRT: Endosomal Sorting Complexes Required for Transport; GIN: Genomic Instability; MAD2: Mitotic Arrest Deficient 2; MCL1: Myeloid Cell Leukemia sequence 1; MPS1: Monopolar Spindle 1 Kinase; MYT1: MYelin Transcription factor 1; PLK1: Polo Like Kinase 1; PUMA: p53-Upregulated Mediator of Apoptosis; SAC: Spindle Assembly Checkpoint; TAA: Tumor-Associated Antigen.
使用抗有丝分裂药物靶向有丝分裂机制以消除癌细胞是一个有百年历史的概念,在临床上仍被常规用作一线治疗。然而,患者的反应仍然不可预测,药物耐药性限制了这些药物的有效性。癌细胞从药物诱导的有丝分裂阻滞(有丝分裂滑溜)中退出以避免随后的细胞死亡,这被认为是导致这种耐药性的主要机制。对抗有丝分裂药物产生耐药性的肿瘤细胞具有染色体不稳定性(CIN)并且通常是非整倍体。在这篇综述中,我们概述了决定有丝分裂过程中细胞命运的关键机制,以及这些过程如何阻碍抗有丝分裂治疗的效果。此外,我们强调了我们实验室的最新工作,该工作强调了 CEP55 在保护非整倍体细胞免于死亡中的功能作用。我们还讨论了在体内靶向 CEP55 的合理性,这可能被证明是一种新的有效治疗策略,可使细胞对微管抑制剂敏感,并可能显著改善患者的预后。缩写词:APC/C:有丝分裂促进复合物/周期蛋白;BAD:BCL2 相关细胞死亡的激动剂;BAK1:BCL2 拮抗剂激酶 1;BAX:BCL2 相关 X;BCL2:B 细胞慢性淋巴细胞白血病(CLL)/淋巴瘤 2;BH:BCL2 同源结构域;BID:BH3 相互作用结构域死亡激动剂;BIM:BCL2 相互作用介导的细胞死亡调节剂;BUB:无苯并咪唑抑制的芽殖;CDC:细胞分裂周期;CDH1:钙粘蛋白-1;CDK1:细胞周期蛋白依赖性激酶 1;CEP55:中心体蛋白(55 kDa):CIN:染色体不稳定性;CTA:癌症睾丸抗原;EGR1:早期生长反应蛋白 1;ERK:细胞外信号调节激酶;ESCRT:内体分选复合物所需运输;GIN:基因组不稳定性;MAD2:有丝分裂阻滞缺陷 2;MCL1:髓细胞白血病序列 1;MPS1:单极纺锤体 1 激酶;MYT1:髓鞘转录因子 1;PLK1:Polo 样激酶 1;PUMA:p53 上调的凋亡介质;SAC:纺锤体组装检查点;TAA:肿瘤相关抗原。