Mechanical shear flow regulates the malignancy of colorectal cancer cells.

Yu-Ting Tseng, Ching-Chung Tsai, Ping-Chen Chen, Bo-Yan Lin, S. C. Hsu, Shu-Ping Huang, Bin Huang
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Abstract

Colorectal cancer (CRC) is notable for its high mortality and high metastatic characteristics. The shear force generated by bloodstream provides mechanical signals regulating multiple responses of cells, including metastatic cancer cells, dispersing in blood vessels. We, therefore, studied the effect of shear flow on circulating CRC cells in the present study. The CRC cell line SW620 was subjected to shear flow of 12.5 dynes/cm2 for 1 and 2 h separately. Resulting elevated caspase-9 and -3 indicated that shear flow initiated the apoptosis of SW620. Enlarged cell size associated with a higher level of cyclin D1 was coincident with the flow cytometric results indicating that the cell cycle was arrested at the G1 phase. An elevated phosphor-eNOSS1177 increased the production of nitric oxide and led to reactive oxygen species-mediated oxidative stress. Shear flow also regulated epithelial-mesenchymal transition (EMT) by increasing E-cadherin and ZO-1 while decreasing Snail and Twist1. The migration and invasion of sheared SW620 were also substantially decreased. Further investigations showed that mitochondrial membrane potential was significantly decreased, whereas mitochondrial mass and ATP production were not changed. In addition to the shear flow of 12.5 dynes/cm2, the expressions of EMT were compared at lower (6.25 dynes/cm2) and at higher (25 dynes/cm2) shear flow. The results showed that lower shear flow increased mesenchymal characteristics and higher shear flow increased epithelial characteristics. Shear flow reduces the malignancy of CRC in their metastatic dispersal that opens up new ways to improve cancer therapies by applying a mechanical shear flow device.
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机械剪切流调节结直肠癌细胞的恶性程度。
结肠直肠癌(CRC)以其高死亡率和高转移性而闻名。血液产生的剪切力提供了机械信号,可调节分散在血管中的细胞(包括转移癌细胞)的多种反应。因此,我们在本研究中研究了剪切力对循环中的 CRC 细胞的影响。将 CRC 细胞株 SW620 分别置于 12.5 达因/平方厘米的剪切流中 1 小时和 2 小时。结果显示,caspase-9和-3的升高表明剪切流引发了SW620细胞的凋亡。细胞体积增大,细胞周期蛋白 D1 水平升高,这与流式细胞仪的结果一致,表明细胞周期停滞在 G1 阶段。磷酸-eNOSS1177 的升高增加了一氧化氮的产生,导致了活性氧介导的氧化应激。剪切流还通过增加 E-cadherin 和 ZO-1 而减少 Snail 和 Twist1 来调节上皮-间质转化(EMT)。剪切SW620的迁移和侵袭也大大减少。进一步的研究表明,线粒体膜电位显著降低,而线粒体质量和 ATP 产量没有变化。除了 12.5 达因/平方厘米的剪切流外,还比较了较低(6.25 达因/平方厘米)和较高(25 达因/平方厘米)剪切流下 EMT 的表达。结果显示,较低的剪切流增加了间质特征,而较高的剪切流增加了上皮特征。剪切流降低了癌细胞转移扩散的恶性程度,这为应用机械剪切流装置改进癌症疗法开辟了新途径。
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