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Store Operated Calcium Entry in Cell Migration and Cancer Metastasis

期刊

CELLS
卷 10, 期 5, 页码 -

出版社

MDPI
DOI: 10.3390/cells10051246

关键词

cell migration; STIM1; orai1; store-operated Ca2+ entry; Ca2+ signaling; focal adhesions; polarization; cancer; metastasis

资金

  1. Biomedical Research Program (BMRP) at Weill Cornell Medicine Qatar - Qatar Foundation
  2. Qatar National Research Fund [NPRP12S-0212-190074, PPM 04-0128-200015, NPRP13S-0206-200274]

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Ca2+ signaling is crucial for cell migration, with a focus on the diverse functions of SOCE pathway. While SOCE has been implicated in regulating focal adhesion turnover, its role in other aspects of cell migration remains less well-defined and requires further research.
Ca2+ signaling is ubiquitous in eukaryotic cells and modulates many cellular events including cell migration. Directional cell migration requires the polarization of both signaling and structural elements. This polarization is reflected in various Ca2+ signaling pathways that impinge on cell movement. In particular, store-operated Ca2+ entry (SOCE) plays important roles in regulating cell movement at both the front and rear of migrating cells. SOCE represents a predominant Ca2+ influx pathway in non-excitable cells, which are the primary migrating cells in multicellular organisms. In this review, we summarize the role of Ca2+ signaling in cell migration with a focus on SOCE and its diverse functions in migrating cells and cancer metastasis. SOCE has been implicated in regulating focal adhesion turnover in a polarized fashion and the mechanisms involved are beginning to be elucidated. However, SOCE is also involved is other aspects of cell migration with a less well-defined mechanistic understanding. Therefore, much remains to be learned regarding the role and regulation of SOCE in migrating cells.

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