期刊
CANCER LETTERS
卷 336, 期 2, 页码 390-397出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2013.03.026
关键词
Store-operated Ca2+ entry; Nasopharyngeal carcinoma; Migration; Metastasis
类别
资金
- Ministry of Education, Culture, Sports, Science and Technology in Japan
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. (C) 2013 Published by Elsevier Ireland Ltd.
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