Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells

Store-operated calcium entry (SOCE) provided through channels formed by ORAI proteins is a major regulator of several cellular processes. In immune cells, it controls fundamental processes such as proliferation, cell adhesion, and migration, while in cancer, SOCE and <i>ORAI1</i> gene ex...

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Autores principales: Alexandre Bokhobza, Nathalie Ziental-Gelus, Laurent Allart, Oksana Iamshanova, Fabien Vanden Abeele
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:a98aa145651c4e9bbc1efdb7fa6715ba2021-11-25T17:10:27ZImpact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells10.3390/cells101130162073-4409https://doaj.org/article/a98aa145651c4e9bbc1efdb7fa6715ba2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3016https://doaj.org/toc/2073-4409Store-operated calcium entry (SOCE) provided through channels formed by ORAI proteins is a major regulator of several cellular processes. In immune cells, it controls fundamental processes such as proliferation, cell adhesion, and migration, while in cancer, SOCE and <i>ORAI1</i> gene expression are dysregulated and lead to abnormal migration and/or cell proliferation. In the present study, we used the CRISPR/Cas9 technique to delete the <i>ORAI1</i> gene and to identify its role in proliferative and migrative properties of the model cell line HEK-293. We showed that ORAI1 deletion greatly reduced SOCE. Thereby, we found that this decrease and the absence of ORAI1 protein did not affect HEK-293 proliferation. In addition, we determined that ORAI1 suppression did not affect adhesive properties but had a limited impact on HEK-293 migration. Overall, we showed that ORAI1 and SOCE are largely dispensable for cellular proliferation, migration, and cellular adhesion of HEK-293 cells. Thus, despite its importance in providing Ca<sup>2+</sup> entry in non-excitable cells, our results indicate that the lack of SOCE does not deeply impact HEK-293 cells. This finding suggests the existence of compensatory mechanism enabling the maintenance of their physiological function.Alexandre BokhobzaNathalie Ziental-GelusLaurent AllartOksana IamshanovaFabien Vanden AbeeleMDPI AGarticlecalciumORAI proteinstore-operated calcium entryproliferationmigrationadhesionBiology (General)QH301-705.5ENCells, Vol 10, Iss 3016, p 3016 (2021)
institution DOAJ
collection DOAJ
language EN
topic calcium
ORAI protein
store-operated calcium entry
proliferation
migration
adhesion
Biology (General)
QH301-705.5
spellingShingle calcium
ORAI protein
store-operated calcium entry
proliferation
migration
adhesion
Biology (General)
QH301-705.5
Alexandre Bokhobza
Nathalie Ziental-Gelus
Laurent Allart
Oksana Iamshanova
Fabien Vanden Abeele
Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells
description Store-operated calcium entry (SOCE) provided through channels formed by ORAI proteins is a major regulator of several cellular processes. In immune cells, it controls fundamental processes such as proliferation, cell adhesion, and migration, while in cancer, SOCE and <i>ORAI1</i> gene expression are dysregulated and lead to abnormal migration and/or cell proliferation. In the present study, we used the CRISPR/Cas9 technique to delete the <i>ORAI1</i> gene and to identify its role in proliferative and migrative properties of the model cell line HEK-293. We showed that ORAI1 deletion greatly reduced SOCE. Thereby, we found that this decrease and the absence of ORAI1 protein did not affect HEK-293 proliferation. In addition, we determined that ORAI1 suppression did not affect adhesive properties but had a limited impact on HEK-293 migration. Overall, we showed that ORAI1 and SOCE are largely dispensable for cellular proliferation, migration, and cellular adhesion of HEK-293 cells. Thus, despite its importance in providing Ca<sup>2+</sup> entry in non-excitable cells, our results indicate that the lack of SOCE does not deeply impact HEK-293 cells. This finding suggests the existence of compensatory mechanism enabling the maintenance of their physiological function.
format article
author Alexandre Bokhobza
Nathalie Ziental-Gelus
Laurent Allart
Oksana Iamshanova
Fabien Vanden Abeele
author_facet Alexandre Bokhobza
Nathalie Ziental-Gelus
Laurent Allart
Oksana Iamshanova
Fabien Vanden Abeele
author_sort Alexandre Bokhobza
title Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells
title_short Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells
title_full Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells
title_fullStr Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells
title_full_unstemmed Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells
title_sort impact of soce abolition by orai1 knockout on the proliferation, adhesion, and migration of hek-293 cells
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/a98aa145651c4e9bbc1efdb7fa6715ba
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