Objectives The mechanical forces on circulating tumor cells (CTCs) should not be ignored in blood and it is more essential that CTCs can overcome and utilize the mechanical interaction to acquire the ability of distant metastasis. At present there are few studies on how suspension mechanics regulates the behavior of tumor cells. The aim of the study was to explore the effects of suspension state on the epithelial–mesenchymal transition (EMT) and stemness of breast CTCs and the molecular mechanisms involved. Results Suspension state could regulate the program of EMT in breast cancer cells, which supported the complex dynamic concept of EMT. It is that the Ras homolog family member A (RhoA)/Rho-associated coiled-coil containing protein kinase 1 (ROCK1) signaling pathway was activated by suspension state in MCF-7 cells instead of MDA-MB-231 cells. In addition, suspension state increased the stemness of breast cancer cells from different aspects. Conclusion The study highlighted the emergence of hybrid epithelial/mesenchymal (E/M) state during hematogenous metastasis and the plasticity of CTCs caused by cancer stem cells, further providing novel insights into clinical monitoring of CTCs and therapeutic strategies.

中文翻译：

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悬浮状态调节乳腺肿瘤细胞的上皮间质转化和干性

目的循环肿瘤细胞（CTCs）的机械力在血液中不容忽视，更重要的是CTCs能够克服并利用机械相互作用获得远处转移的能力。目前关于悬浮力学如何调节肿瘤细胞行为的研究很少。该研究的目的是探索悬浮状态对乳腺 CTC 的上皮间质转化 (EMT) 和干性的影响以及所涉及的分子机制。结果悬浮状态可以调节乳腺癌细胞EMT的程序，支持EMT的复杂动态概念。Ras 同源家族成员 A (RhoA)/Rho 相关卷曲螺旋含有蛋白激酶 1 (ROCK1) 信号通路在 MCF-7 细胞而不是 MDA-MB-231 细胞中被悬浮状态激活。此外，悬浮状态从不同方面增加了乳腺癌细胞的干性。结论 该研究强调了血行转移过程中混合上皮/间充质 (E/M) 状态的出现和癌症干细胞引起的 CTC 的可塑性，进一步为 CTC 的临床监测和治疗策略提供了新的见解。