Mechanisms of ploidy increase in human cancers: a new role for cell cannibalism.
Mechanisms of ploidy increase in human cancers: a new role for cell cannibalism.
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DOI：
10.1158/0008-5472.can-11-3127
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发表时间：
2012-04-01
期刊：
影响因子：
11.2
通讯作者：
Overholtzer M
中科院分区：
文献类型：
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作者：
Krajcovic M;Overholtzer M
非整倍性是人类癌症的标志，其起源于异常的有丝分裂。许多非整倍体癌细胞也具有大于二倍体的DNA含量，这表明多倍体是肿瘤进展期间非整倍体的常见前兆。多倍体细胞可以起源于细胞融合、胞内复制和胞质分裂失败。最近，我们发现，细胞自食的内吞，一种形式的细胞吞噬涉及活细胞，也导致多倍体，因为内化的细胞破坏胞质分裂的吞噬细胞宿主。通过这种机制，同类相食的细胞行为可以通过导致非整倍体来促进肿瘤进展。在这里，我们讨论了癌症中的细胞自相残杀和导致多倍体癌细胞形成的其他机制。
Aneuploidy is a hallmark of human cancers that originates from abnormal mitoses. Many aneuploid cancer cells also have greater-than-diploid DNA content, suggesting that polyploidy is a common precursor to aneuploidy during tumor progression. Polyploid cells can originate from cell fusion, endoreplication, and cytokinesis failure. Recently we found that cell cannibalism by entosis, a form of cell engulfment involving live cells, also leads to polyploidy, as internalized cells disrupt cytokinesis of their engulfing cell hosts. By this mechanism, cannibalistic cell behavior could promote tumor progression by leading to aneuploidy. Here we discuss cell cannibalism in cancer and other mechanisms that result in the formation of polyploid cancer cells.