乳腺癌细胞的迁移是死亡的主要原因，并受到细胞外基质（ECM）物理因素的显着调节。具体来说，我们发现ECM的曲率和刚度可以有效引导细胞迁移的速度和方向。然而，目前尚不清楚这些双重物理因素调节细胞迁移时的影响程度如何。此外，分子水平上乳腺癌细胞迁移的力学生物学机制和细胞牵引力（CTF）的分析也很重要，但缺乏系统的研究。因此，我们采用微流控平台构建具有独立可调曲率和刚度的水凝胶微球作为乳腺癌细胞迁移的三维基质。我们发现细胞迁移速度与曲率呈负相关，与刚度呈正相关。此外，还研究了曲率对粘着斑表达以及 F-肌动蛋白在分子水平上的分配的影响。此外，在电机离合器数学模型和水凝胶微球应力传感器的帮助下，得出的结论是，细胞感知物理因素（曲率和刚度）导致CTF变化，最终调节细胞运动。总之，我们采用理论模型（电机离合器）和实验策略（应力传感器）来了解曲率和刚度调节乳腺癌细胞运动的机制。这些结果提供了ECM物理因素驱动癌细胞迁移的证据，并从力学生物学的角度解释了其机制。

The migration of breast cancer cells is the main cause of death and significantly regulated by physical factors of the extracellular matrix (ECM). To be specific, the curvature and stiffness of the ECM were discovered to effectively guide cell migration in velocity and direction. However, it is not clear what the extent of effect is when these dual-physical factors regulate cell migration. Moreover, the mechanobiology mechanism of breast cancer cell migration in the molecular level and analysis of cell traction force (CTF) are also important, but there is a lack of systematic investigation. Therefore, we employed a microfluidic platform to construct hydrogel microspheres with an independently adjustable curvature and stiffness as a three-dimensional substrate for breast cancer cell migration. We found that the cell migration velocity was negatively correlated to curvature and positively correlated to stiffness. In addition, curvature was investigated to influence the focal adhesion expression as well as the assignment of F-actin at the molecular level. Further, with the help of a motor-clutch mathematical model and hydrogel microsphere stress sensors, it was concluded that cells perceived physical factors (curvature and stiffness) to cause changes in CTF, which ultimately regulated cell motility. In summary, we employed a theoretical model (motor-clutch) and experimental strategy (stress sensors) to understand the mechanism of curvature and stiffness regulating breast cancer cell motility. These results provide evidence of force driven cancer cell migration by ECM physical factors and explain the mechanism from the perspective of mechanobiology.