STIM1 signals through NFAT1 independently of Orai1 and SOCE to regulate breast cancer cell migration.

Breast cancer Cell migration Invasion Metastatic NFAT Orai1 STIM1 Store-operated calcium entry

Journal

Cell calcium
ISSN: 1532-1991
Titre abrégé: Cell Calcium
Pays: Netherlands
ID NLM: 8006226

Informations de publication

Date de publication:
Sep 2023
Historique:
received: 27 03 2023
revised: 25 06 2023
accepted: 27 06 2023
pubmed: 4 7 2023
medline: 4 7 2023
entrez: 3 7 2023
Statut: ppublish

Résumé

Store-operated calcium entry (SOCE) contributes to several physiological and pathological conditions including transcription, secretion, immunodeficiencies, and cancer. SOCE has been shown to be important for breast cancer cell migration where knockdown of SOCE components (STIM1 or Orai1) decreases cancer metastasis. Here we show unexpectedly that complete knockout of STIM1 (STIM1-KO) using gene editing in metastatic MDA-MB-231 breast cancer cells results in faster migration and enhanced invasion capacity. In contrast, Orai1-KO cells, which have similar levels of SOCE inhibition as STIM1-KO, migrate slower than the parental cell line. This shows that the enhanced migration phenotype of STIM1-KO cells is not due to the loss of Ca

Identifiants

pubmed: 37399784
pii: S0143-4160(23)00091-X
doi: 10.1016/j.ceca.2023.102779
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102779

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare no competing interests.

Auteurs

Ayat S Hammad (AS)

College of Health and Life Science, Hamad bin Khalifa University, Doha, Qatar; Calcium Signaling Group, Research Department, Weill Cornell Medicine, Doha, Qatar.

Fang Yu (F)

Calcium Signaling Group, Research Department, Weill Cornell Medicine, Doha, Qatar; Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, United States.

Jawaher Al-Hamaq (J)

Calcium Signaling Group, Research Department, Weill Cornell Medicine, Doha, Qatar.

F David Horgen (FD)

Department of Natural Sciences, Hawaii Pacific University, Honolulu, Hawaii, United States.

Khaled Machaca (K)

Calcium Signaling Group, Research Department, Weill Cornell Medicine, Doha, Qatar; Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, United States. Electronic address: khm2002@qatar-med.cornell.edu.

Classifications MeSH