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首页> 外文期刊>Neoplasia: an international journal for oncology research >Polyploidy Formation in Doxorubicin-Treated Cancer Cells Can Favor Escape from Senescence
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Polyploidy Formation in Doxorubicin-Treated Cancer Cells Can Favor Escape from Senescence

机译：在多肠蛋白处理的癌细胞中的多倍体形成可以利用衰老逃逸

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Cancer cells can undergo stress-induced premature senescence, which is considered to be a desirable outcome of anticancer treatment. However, the escape from senescence and cancer cell repopulation give rise to some doubts concerning the effectiveness of the senescence-induced anticancer therapy. Similarly, it is postulated that polyploidization of cancer cells is connected with disease relapse. We postulate that cancer cell polyploidization associated with senescence is the culprit of atypical cell divisions leading to cancer cell regrowth. Accordingly, we aimed to dissociate between these two phenomena. We induced senescence in HCT 116 cells by pulse treatment with doxorubicin and observed transiently increased ploidy, abnormal nuclear morphology, and various distributions of some proteins (e.g., p21, Ki-67, SA-β-galactosidase) in the subnuclei. Doxorubicin-treated HCT 116 cells displayed an increased production of reactive oxygen species (ROS) possibly caused by an increased amount of mitochondria, which are characterized by low membrane potential. A decrease in the level of ROS by Trolox partially protected the cells from polyploidization but not from senescence. Interestingly, a decreased level of ROS prevented the cells from escaping senescence. We also show that MCF7 cells senesce, but this is not accompanied by the increase of ploidy upon doxorubicin treatment. Moreover, they were stably growth arrested, thus proving that polyploidy but not senescence per se enables to regain the ability to proliferate. Our preliminary results indicate that the different propensity of the HCT 116 and MCF7 cells to increase ploidy upon cell senescence could be caused by a different level of the mTOR and/or Pim-1 kinases.
机译：癌细胞可以进行应激诱导的过早衰老，这被认为是抗癌治疗的理想结果。然而，衰老和癌细胞重新迁移的逃避引起了一些关于衰老诱导的抗癌治疗的有效性的疑虑。类似地，假设癌细胞的多倍化与疾病复发相关。我们假设与衰老相关的癌细胞多倍化是非典型细胞分裂的罪魁祸首，导致癌细胞再生。因此，我们的目标是在这两种现象之间解散。我们通过用多柔比星进行脉冲处理在HCT116细胞中诱导衰老，并观察到亚核中的一些蛋白质（例如，P21，Ki-67，Sa-β-半乳糖苷酶的各种分布增加的倍率增加，异常核形态和各种分布。 Doxorubicin治疗的HCT 116细胞显示出可能由增加的线粒体量引起的反应性氧物质（ROS）的增加，其特征在于低膜电位。通过滴鼻菌的RO水平降低，部分保护细胞免受多倍化的细胞，但不是从衰老。有趣的是，RO水平降低阻止细胞逸出了衰老。我们还表明MCF7细胞Senesce，但这并不伴随着对多柔比蛋白治疗的倍率的增加。此外，它们被稳定的生长被捕，从而证明多倍体但不是衰老，可以恢复增殖的能力。我们的初步结果表明，在细胞衰老时，HCT116和MCF7细胞增加倍率的不同倾向可能是由MTOR和/或PIM-1激酶的不同水平引起的。

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