肌球蛋白-II依赖的细胞收缩有助于间皮瘤细胞自发结节形成
Myosin-II dependent cell contractility contributes to spontaneous nodule formation of mesothelioma cells
摘要：
我们证明，特征结节出现在几个恶性胸膜间皮瘤（MPM）细胞系的文化。而不是过度的局部细胞增殖，结节产生肌球蛋白II驱动的细胞收缩。聚集过程可以通过合适的肌动球蛋白收缩性的药理学抑制剂来预防或逆转。多细胞图案化过程的细胞分辨弹塑性模型表明，结节的形态和大小以及它们形成的速度是由细胞施加在其邻居上的机械张力和细胞-基质粘附复合物的稳定性决定的。一个均匀的，自张麦克斯韦流体的线性稳定性分析表明无条件存在的图案不稳定性。
英文摘要：
We demonstrate that characteristic nodules emerge in cultures of several malignant pleural mesothelioma (MPM) cell lines. Instead of excessive local cell proliferation, the nodules arise by Myosin II-driven cell contractility. The aggregation process can be prevented or reversed by suitable pharmacological inhibitors of acto-myosin contractility. A cell-resolved elasto-plastic model of the multicellular patterning process indicates that the morphology and size of the nodules as well as the speed of their formation is determined by the mechanical tension cells exert on their neighbors, and the stability of cell-substrate adhesion complexes. A linear stability analysis of a homogenous, self-tensioned Maxwell fluid indicates the unconditional presence of a patterning instability.
机构、总结、中文摘要均由AI分析而来，可能存在错误，请以论文正文为准。
