Huang Xuan, Dai Wei, Darzynkiewicz Zbigniew
Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA.
Cell Cycle. 2005 Jun;4(6):801-5. doi: 10.4161/cc.4.6.1695. Epub 2005 Jun 15.
Cells of epithelial or endothelial lineage when forced to grow in suspension undergo the detachment-induced death termed "anoikis". In the present study we explored the reverse situation namely the effect of enforcement of hematopoietic lineage cells that are normally maintained in suspension to grow attached. Towards this end murine L1210 or human HL-60 and Jurkat leukemia cells were cultured in slide chambers coated with poly-L- or poly-D- lysine, or with compound 48/80, the polycations attracting them electrostatically. Within minutes after the transfer L1210 cells strongly adhered to bottom surface of the dish and shortly thereafter binuclear-, and later on, polynuclear-cells become apparent. The frequency of nuclei per cell was increasing with time and polykaryons with up to 16 nuclei and high DNA ploidy (DI = 16.0) were apparent after 48 h. After 4 days the size (volume) of some polykaryons exceeded by over 340-fold the volume of mononuclear cells. The presence of mitotic figures and abnormal mitotic spindles in adhering polykaryons provided evidence of the impeded cytokinesis that led to endomitosis. Most polykaryons excluded trypan blue, had balanced growth (unchanged protein/DNA ratio compared to monokaryons), and showed no evidence of apoptosis. Individual nuclei within each polykaryon replicated DNA in synchrony. The strong cell attachment and aborted cytokinesis were cell line specific since no significant endomitosis was observed in Jurkat- or HL-60- cells which did not strongly attach to polycation-coated surfaces. Defective cytokinesis and induction of polyploidy by this mechanism, if occurs in vivo (e.g., mediated by integrins), may lead to aneuploidy and therefore have tumorigenic consequences. The phenomenon offers novel experimental model for induction of polyploidy and provides alternative to cytocholasin B to prevent cytokinesis in the mutagenicity cytokinesis-blocked micronucleus (CBMN) assay.
上皮或内皮谱系的细胞在被迫悬浮生长时会经历称为“失巢凋亡”的脱离诱导死亡。在本研究中,我们探讨了相反的情况,即强制通常维持悬浮生长的造血谱系细胞贴壁生长的影响。为此,将小鼠L1210或人HL-60和Jurkat白血病细胞培养在涂有聚-L-赖氨酸或聚-D-赖氨酸或化合物48/80的玻片培养室中,这些聚阳离子通过静电吸引它们。转移后几分钟内,L1210细胞强烈粘附于培养皿底面,此后不久双核细胞出现,随后多核细胞也变得明显。每个细胞中的核频率随时间增加,48小时后出现多达16个核且具有高DNA倍性(DI = 16.0)的多核体。4天后,一些多核体的大小(体积)比单核细胞的体积大超过340倍。粘附的多核体中存在有丝分裂图和异常有丝分裂纺锤体,这提供了导致核内有丝分裂的胞质分裂受阻的证据。大多数多核体排斥台盼蓝,具有平衡生长(与单核细胞相比蛋白质/DNA比率不变),并且没有凋亡迹象。每个多核体内的单个核同步复制DNA。强烈的细胞粘附和胞质分裂失败是细胞系特异性的,因为在未强烈粘附于聚阳离子包被表面的Jurkat或HL-60细胞中未观察到明显的核内有丝分裂。如果这种机制在体内发生(例如由整合素介导),有缺陷的胞质分裂和多倍体的诱导可能导致非整倍体,因此具有致瘤后果。该现象为多倍体的诱导提供了新的实验模型,并为在诱变性胞质分裂阻断微核(CBMN)试验中防止胞质分裂提供了细胞松弛素B的替代方法。