White Carl
Physiology and Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, United States.
Front Oncol. 2017 Aug 10;7:171. doi: 10.3389/fonc.2017.00171. eCollection 2017.
Cell migration is one of the many processes orchestrated by calcium (Ca) signaling, and its dysregulation drives the increased invasive and metastatic potential of cancer cells. The ability of Ca to function effectively as a regulator of migration requires the generation of temporally complex signals within spatially restricted microdomains. The generation and maintenance of these Ca signals require a specific structural architecture and tightly regulated communication between the extracellular space, intracellular organelles, and cytoplasmic compartments. New insights into how Ca microdomains are shaped by interorganellar Ca communication have shed light on how Ca coordinates cell migration by directing cellular polarization and the rearrangement of structural proteins. Importantly, we are beginning to understand how cancer subverts normal migration through the activity of oncogenes and tumor suppressors that impinge directly on the physiological function or expression levels of Ca signaling proteins. In this review, we present and discuss research at the forefront of interorganellar Ca signaling as it relates to cell migration, metastasis, and cancer progression, with special focus on endoplasmic reticulum-to-mitochondrial Ca transfer.
细胞迁移是由钙（Ca）信号调控的众多过程之一，其失调会导致癌细胞侵袭和转移潜能增加。Ca要有效地发挥迁移调节因子的作用，需要在空间受限的微区内产生时间上复杂的信号。这些Ca信号的产生和维持需要特定的结构架构以及细胞外空间、细胞内细胞器和细胞质区室之间严格调控的通讯。关于细胞内细胞器间Ca通讯如何塑造Ca微区的新见解，揭示了Ca如何通过引导细胞极化和结构蛋白重排来协调细胞迁移。重要的是，我们开始了解癌症如何通过直接影响Ca信号蛋白生理功能或表达水平的癌基因和肿瘤抑制因子的活性来颠覆正常迁移。在本综述中，我们展示并讨论了细胞内细胞器间Ca信号前沿研究，这些研究与细胞迁移、转移和癌症进展相关，特别关注内质网到线粒体的Ca转运。
