To undergo mitosis successfully, most animal cells need to acquire a round shape to provide space for the mitotic spindle. This mitotic rounding relies on mechanical deformation of surrounding tissue and is driven by forces emanating from actomyosin contractility. Cancer cells are able to maintain successful mitosis in mechanically challenging environments such as the increasingly crowded environment of a growing tumor, thus, suggesting an enhanced ability of mitotic rounding in cancer. Here, it is shown that the epithelial–mesenchymal transition (EMT), a hallmark of cancer progression and metastasis, gives rise to cell‐mechanical changes in breast epithelial cells. These changes are opposite in interphase and mitosis and correspond to an enhanced mitotic rounding strength. Furthermore, it is shown that cell‐mechanical changes correlate with a strong EMT‐induced change in the activity of Rho GTPases RhoA and Rac1. Accordingly, it is found that Rac1 inhibition rescues the EMT‐induced cortex‐mechanical phenotype. The findings hint at a new role of EMT in successful mitotic rounding and division in mechanically confined environments such as a growing tumor.

中文翻译：

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EMT 诱导的细胞机械变化增强有丝分裂变圆强度

为了成功进行有丝分裂，大多数动物细胞需要形成圆形，为有丝分裂纺锤体提供空间。这种有丝分裂变圆依赖于周围组织的机械变形，并由肌动球蛋白收缩性产生的力驱动。癌细胞能够在机械挑战性的环境中维持成功的有丝分裂，例如生长肿瘤的日益拥挤的环境，因此表明癌症中有丝分裂变圆的能力增强。在这里，研究表明上皮-间质转化（EMT）是癌症进展和转移的标志，会引起乳腺上皮细胞的细胞机械变化。这些变化在间期和有丝分裂中是相反的，并且对应于增强的有丝分裂圆化强度。此外，研究表明细胞机械变化与 EMT 诱导的 Rho GTPases RhoA 和 Rac1 活性的强烈变化相关。因此，我们发现 Rac1 抑制可以挽救 EMT 诱导的皮质机械表型。这些发现暗示了 EMT 在机械受限环境（例如生长中的肿瘤）中成功有丝分裂变圆和分裂中的新作用。