Abstract
Store-operated Ca2+ entry (SOCE) is the major pathway of Ca2+ entry in mammalian cells, and regulates a variety of cellular functions including proliferation, motility, apoptosis, and death. Accumulating evidence has indicated that augmented SOCE is related to the generation and development of cancer, including tumor formation, proliferation, angiogenesis, metastasis, and antitumor immunity. Therefore, the development of compounds targeting SOCE has been proposed as a potential and effective strategy for use in cancer therapy. In this review, we summarize the current research on SOCE inhibitors and blockers, discuss their effects and possible mechanisms of action in cancer therapy, and induce a new perspective on the treatment of cancer.
Highlights
The Overview of Store-Operated Calcium EntryStore-operated calcium entry (SOCE) is typically activated by ligands of cell surface receptors such as G proteins that activate phospholipase C (PLC) to cleave phosphatidylinositol 4, 5-bisphosphate (PIP2) and produce inositol 1, 4, 5-trisphosphate (IP3)
Accumulating evidence has shown that stromal interaction molecules (STIMs)/ORAI-mediated Store-operated Ca2+ entry (SOCE) is excessive in cancer tissues, and it is becoming clear that augmented SOCE promotes the malignant behavior of cancer cells, including tumor growth, angiogenesis, and metastasis
Multiple compounds targeting SOCE have been developed and their efficiency in the inhibition of proliferation and migration of cancer cells has been evaluated
Summary
The Overview of Store-Operated Calcium EntryStore-operated calcium entry (SOCE) is typically activated by ligands of cell surface receptors such as G proteins that activate phospholipase C (PLC) to cleave phosphatidylinositol 4, 5-bisphosphate (PIP2) and produce inositol 1, 4, 5-trisphosphate (IP3). As a SOCE inhibitor, SKF 96365 was reported to inhibit cell proliferation in many cancers by inducing cell apoptosis and cell cycle arrest in G2/M phase (Nordström et al, 1992; Lee et al, 1993; Arias-Montaño et al, 1998; Cai et al, 2009; Zeng et al, 2013; Zhang et al, 2015; Jing et al, 2016; Wang W. et al, 2018).
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