Inhibition of store-operated Ca2+ entry suppresses EGF-induced migration and eliminates extravasation from vasculature in nasopharyngeal carcinoma cell
- Authors
- Zhang, J., Wei, J., Kanada, M., Yan, L., Zhang, Z., Watanabe, H., and Terakawa, S.
- ID
- ZDB-PUB-130604-5
- Date
- 2013
- Source
- Cancer letters 336(2): 390-7 (Journal)
- Registered Authors
- Keywords
- store-operated Ca2+ entry, nasopharyngeal carcinoma, migration, metastasis
- MeSH Terms
-
- Cell Movement/drug effects
- Cell Movement/physiology
- Ion Transport
- Epidermal Growth Factor/metabolism*
- Humans
- Calcium Channel Blockers/pharmacology
- Membrane Proteins/metabolism*
- Calcium Signaling/drug effects
- Calcium Signaling/physiology*
- Animals, Genetically Modified
- Animals
- Signal Transduction
- Nasopharyngeal Neoplasms/blood supply*
- Nasopharyngeal Neoplasms/metabolism
- Nasopharyngeal Neoplasms/pathology
- Nasopharyngeal Neoplasms/therapy
- Cell Line, Tumor
- Zebrafish
- Calcium/metabolism*
- PubMed
- 23623984 Full text @ Cancer Lett.
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.