Inhibition of store-operated Ca2+ entry suppresses EGF-induced migration and eliminates extravasation from vasculature in nasopharyngeal carcinoma cell

•It was demonstrated that SOCE is a predominant Ca2+ signaling for NPC cell metastasis.•A zebrafish hematogenous metastasis model was recruited for the investigation of NPC cell metastasis.•For the first time, the dynamic extravasation of NPC cells from vasculature was visually observed.

Store-operated Ca2+ entry (SOCE) mediates Ca2+ responses evoked by extracellular signaling molecules to promote increases in cytosolic Ca2+, thereby triggering downstream signal transduction. Here we demonstrated that either the pharmacological blockage of Ca2+ influx through SOCE or the knockdown of Orai1, a key molecule of SOCE, suppressed the epidermal growth factor-induced migration by disturbing Ca2+ signaling in nasopharyngeal carcinoma (NPC) cell. Furthermore, Orai1 depletion led to a delayed cell attachment to the extracellular matrix surface in vitro and eliminated the extravasation of microinjected cells from vasculature in a zebrafish hematogenous metastasis model. Our findings thus indicate that SOCE acts as a predominant Ca2+ signaling involved in NPC cell metastasis, and may serve as a candidate target for anti-metastasis therapy in NPC.