Regulation of invadopodia by mechanical signaling.
Regulation of invadopodia by mechanical signaling.
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DOI：
10.1016/j.yexcr.2015.10.038
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发表时间：
2016-04-10
影响因子：
3.7
通讯作者：
Weaver AM
中科院分区：
文献类型：
--
作者：
Parekh A;Weaver AM
肿瘤微环境中的机械刚性与肿瘤形成和侵袭性的高风险相关。由刚性微环境驱动的基于粘附的信号传导被认为促进癌细胞从原发性肿瘤侵袭和迁移。细胞外基质（ECM）的蛋白水解降解是该过程的关键组成部分，并由亚细胞富含肌动蛋白的结构（称为侵袭伪足）介导。ECM刚性和细胞牵引应力促进侵袭伪足的形成和活动，这表明这些结构在机械传感中的作用。机械敏感性粘合剂和信号传导组分在侵入伪足的存在和活性进一步表明这些结构利用肌球蛋白依赖性力量来探测和重塑其ECM环境的潜力。在这里，我们提供了一个简短的审查的作用，粘附为基础的机械信号在控制侵袭性伪足和侵袭性癌症的行为。
Mechanical rigidity in the tumor microenvironment is associated with a high risk of tumor formation and aggressiveness. Adhesion-based signaling driven by a rigid microenvironment is thought to facilitate invasion and migration of cancer cells away from primary tumors. Proteolytic degradation of extracellular matrix (ECM) is a key component of this process and is mediated by subcellular actin-rich structures known as invadopodia. Both ECM rigidity and cellular traction stresses promote invadopodia formation and activity, suggesting a role for these structures in mechanosensing. The presence and activity of mechanosensitive adhesive and signaling components at invadopodia further indicates the potential for these structures to utilize myosin-dependent forces to probe and remodel their ECM environments. Here, we provide a brief review of the role of adhesion-based mechanical signaling in controlling invadopodia and invasive cancer behavior.