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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-opera... Full description

Journal Title: Cancer Letters 19 August 2013, Vol.336(2), pp.390-397
Main Author: Zhang, Jinyan
Other Authors: Wei, Jiazhang , Kanada, Masamitsu , Yan, Libo , Zhang, Zhe , Watanabe, Hiroshi , Terakawa, Susumu
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0304-3835 ; E-ISSN: 1872-7980 ; DOI: 10.1016/j.canlet.2013.03.026
Link: http://dx.doi.org/10.1016/j.canlet.2013.03.026
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recordid: elsevier_sdoi_10_1016_j_canlet_2013_03_026
title: Inhibition of store-operated Ca2+ entry suppresses EGF-induced migration and eliminates extravasation from vasculature in nasopharyngeal carcinoma cell
format: Article
creator:
  • Zhang, Jinyan
  • Wei, Jiazhang
  • Kanada, Masamitsu
  • Yan, Libo
  • Zhang, Zhe
  • Watanabe, Hiroshi
  • Terakawa, Susumu
subjects:
  • Store-Operated Ca2+ Entry
  • Nasopharyngeal Carcinoma
  • Migration
  • Metastasis
  • Store-Operated Ca2+ Entry
  • Nasopharyngeal Carcinoma
  • Migration
  • Metastasis
  • Medicine
ispartof: Cancer Letters, 19 August 2013, Vol.336(2), pp.390-397
description: •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....
language: eng
source:
identifier: ISSN: 0304-3835 ; E-ISSN: 1872-7980 ; DOI: 10.1016/j.canlet.2013.03.026
fulltext: fulltext
issn:
  • 0304-3835
  • 03043835
  • 1872-7980
  • 18727980
url: Link


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titleInhibition of store-operated Ca2+ entry suppresses EGF-induced migration and eliminates extravasation from vasculature in nasopharyngeal carcinoma cell
creatorZhang, Jinyan ; Wei, Jiazhang ; Kanada, Masamitsu ; Yan, Libo ; Zhang, Zhe ; Watanabe, Hiroshi ; Terakawa, Susumu
ispartofCancer Letters, 19 August 2013, Vol.336(2), pp.390-397
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subjectStore-Operated Ca2+ Entry ; Nasopharyngeal Carcinoma ; Migration ; Metastasis ; Store-Operated Ca2+ Entry ; Nasopharyngeal Carcinoma ; Migration ; Metastasis ; Medicine
description•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....
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titleInhibition of store-operated Ca2+ entry suppresses EGF-induced migration and eliminates extravasation from vasculature in nasopharyngeal carcinoma cell
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•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....

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titleInhibition of store-operated Ca2+ entry suppresses EGF-induced migration and eliminates extravasation from vasculature in nasopharyngeal carcinoma cell
authorZhang, Jinyan ; Wei, Jiazhang ; Kanada, Masamitsu ; Yan, Libo ; Zhang, Zhe ; Watanabe, Hiroshi ; Terakawa, Susumu
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•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....

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date2013-08-19