Aurora B抑制在RB和p53缺陷细胞中诱导超多倍体和长期增殖潜能的丧失。

IF 8.1 1区 生物学 Q1 CELL BIOLOGY Cell Death & Disease Pub Date : 2025-01-08 DOI:10.1038/s41419-024-07329-7
Shivam Vora, Saptarshi Chatterjee, Ariel Andrew, Ramyashree Prasanna Kumar, Martina Proctor, Zhen Zeng, Rituparna Bhatt, Deborah Nazareth, Madushan Fernando, Mathew J K Jones, Yaowu He, John D Hooper, Nigel A J McMillan, Jelena Urosevic, Jamal Saeh, Jon Travers, Daniela Cimini, Jing Chen, Brian Gabrielli
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引用次数: 0

摘要

多倍体是化疗的常见结果,但关于多倍体是不利的、良性的还是有利的结果,有相互矛盾的证据。我们发现,Aurora B激酶抑制剂在许多细胞类型中有效地促进多倍体,导致RB和p53功能细胞的细胞周期退出,但在RB和p53功能丧失的细胞中产生超多倍体。这些超多倍体细胞(DNA含量为100 - 8n)是有活力的,但在体外失去了长期增殖潜力,在体内不能形成肿瘤。对这些细胞有丝分裂的研究显示,大量的中心体能够支持有丝分裂的纺锤极,但即使在2-3天后去除AURKB抑制剂,这些中心体也无法进展到后期/末期结构。然而,当1天后去除AURKB抑制剂时,当细胞单胞分裂失败变为四倍体时,它们保留了集落形成能力和长期增殖潜力。多倍体细胞产生可存活子细胞的潜力的数学模型表明,具有bbbb8n DNA和b>4功能纺锤极的细胞产生可存活子细胞的概率接近于零,支持我们的实验观察。这些发现表明肿瘤细胞可以耐受四倍体,但高倍体状态与长期增殖潜力不相容。AURKBi驱动的超多倍体细胞形成和命运模型。Aurora B抑制剂(AURKBi)治疗RB+p53缺陷细胞可有效促进细胞分裂失败。一个失败的细胞分裂产生三种可能的结果:四倍体后代的持续增殖,细胞死亡,或者如果AURKBi持续存在,则高多倍体状态。一旦细胞两次细胞分裂失败,DNA含量达到48n,即使在没有AURKBi的情况下,它们也会继续经历多轮内膜分裂,要么变成可存活的超多倍体,要么死亡。超多倍体细胞没有长期的增殖潜能。
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Aurora B inhibition induces hyper-polyploidy and loss of long-term proliferative potential in RB and p53 defective cells.

Polyploidy is a common outcome of chemotherapies, but there is conflicting evidence as to whether polyploidy is an adverse, benign or even favourable outcome. We show Aurora B kinase inhibitors efficiently promote polyploidy in many cell types, resulting in the cell cycle exit in RB and p53 functional cells, but hyper-polyploidy in cells with loss of RB and p53 function. These hyper-polyploid cells (>8n DNA content) are viable but have lost long-term proliferative potential in vitro and fail to form tumours in vivo. Investigation of mitosis in these cells revealed high numbers of centrosomes that were capable of supporting functional mitotic spindle poles, but these failed to progress to anaphase/telophase structures even when AURKB inhibitor was removed after 2-3 days. However, when AURKB inhibitor was removed after 1 day and cells had failed a single cytokinesis to become tetraploid, they retained colony forming ability and long-term proliferative potential. Mathematical modelling of the potential for polyploid cells to produce viable daughter cells demonstrated that cells with >8n DNA and >4 functional spindle poles approach zero probability of a viable daughter, supporting our experimental observations. These findings demonstrate that tetraploidy is tolerated by tumour cells, but higher ploidy states are incompatible with long-term proliferative potential. Model for AURKBi driven hyper-polyploid cells formation and fate. Aurora B inhibitor (AURKBi) treatment of RB+p53 defective cells efficiently promotes failed cell division. One failed cell division produces three possible outcomes, continued proliferation of the tetraploid daughter, cell death, or if AURKBi is continued, high polyploid states. Once cell have failed cell division >twice and have >8n DNA content they will continue to undergo rounds of endomitosis even in the absence of AURKBi to either become viable hyper-polyploid or die. The hyper-polyploid cells have no long-term proliferative potential.

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来源期刊
Cell Death & Disease
Cell Death & Disease CELL BIOLOGY-
CiteScore
15.10
自引率
2.20%
发文量
935
审稿时长
2 months
期刊介绍: Brought to readers by the editorial team of Cell Death & Differentiation, Cell Death & Disease is an online peer-reviewed journal specializing in translational cell death research. It covers a wide range of topics in experimental and internal medicine, including cancer, immunity, neuroscience, and now cancer metabolism. Cell Death & Disease seeks to encompass the breadth of translational implications of cell death, and topics of particular concentration will include, but are not limited to, the following: Experimental medicine Cancer Immunity Internal medicine Neuroscience Cancer metabolism
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