Kalkan Batuhan Mert, Ozcan Selahattin Can, Quintyne Nicholas J, Reed Samantha L, Acilan Ceyda
Graduate School of Health Sciences, Koç University, Istanbul 34450, Turkey.
Research Center for Translational Medicine (KUTTAM), Koç University, Istanbul 34450, Turkey.
Cancers (Basel). 2022 Jan 17;14(2):442. doi: 10.3390/cancers14020442.
Aberrations in the centrosome number and structure can readily be detected at all stages of tumor progression and are considered hallmarks of cancer. Centrosome anomalies are closely linked to chromosome instability and, therefore, are proposed to be one of the driving events of tumor formation and progression. This concept, first posited by Boveri over 100 years ago, has been an area of interest to cancer researchers. We have now begun to understand the processes by which these numerical and structural anomalies may lead to cancer, and vice-versa: how key events that occur during carcinogenesis could lead to amplification of centrosomes. Despite the proliferative advantages that having extra centrosomes may confer, their presence can also lead to loss of essential genetic material as a result of segregational errors and cancer cells must deal with these deadly consequences. Here, we review recent advances in the current literature describing the mechanisms by which cancer cells amplify their centrosomes and the methods they employ to tolerate the presence of these anomalies, focusing particularly on centrosomal clustering.
在肿瘤进展的各个阶段，中心体数量和结构的异常都很容易被检测到，并且被认为是癌症的标志。中心体异常与染色体不稳定性密切相关，因此被认为是肿瘤形成和进展的驱动事件之一。这个概念在100多年前由博韦里首次提出，一直是癌症研究人员感兴趣的领域。我们现在已经开始了解这些数量和结构异常可能导致癌症的过程，反之亦然：致癌过程中发生的关键事件如何导致中心体扩增。尽管额外的中心体可能带来增殖优势，但它们的存在也可能由于分离错误导致必需遗传物质的丢失，而癌细胞必须应对这些致命后果。在这里，我们回顾了当前文献中描述癌细胞扩增其中心体的机制以及它们用来耐受这些异常存在的方法的最新进展，特别关注中心体聚集。
