ORAI1 regulates sustained cytosolic free calcium fluctuations during breast cancer cell apoptosis and apoptotic resistance via a STIM1 independent pathway
Abstract Excessive rapid increases in cytosolic free Ca2+ have a clear association with the induction of cancer cell death. Whereas, characterizing the Ca2+ signaling events that occur during the progression of the apoptotic cascade over a period of hours or days, has not yet been possible. Now using genetically encoded Ca2+ indicators complemented with automated epifluorescence microscopy we have shown that staurosporine‐induced apoptosis in MDA‐MB‐231 breast cancer cells was associated with delayed development of cytosolic free Ca2+ fluctuations, which were then maintained for 24 h. These cytosolic free Ca2+ fluctuations were dependent on the Ca2+ channel ORAI1. Silencing of ORAI1, but not its canonical activators STIM1 and STIM2, promoted apoptosis in this model. The pathway for this regulation implicates a mechanism previously associated with the migration of cancer cells involving ORAI1, the chaperone protein SigmaR1, and Ca2+‐activated K+ channels..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:36 |
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| Enthalten in: |
The FASEB Journal - 36(2022), 1 |
| Beteiligte Personen: |
Bassett, John J. [VerfasserIn] |
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| BKL: |
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| Anmerkungen: |
© 2022 Federation of American Societies for Experimental Biology |
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| Umfang: |
15 |
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| doi: |
10.1096/fj.202002031RR |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Abstract Excessive rapid increases in cytosolic free Ca2+ have a clear association with the induction of cancer cell death. Whereas, characterizing the Ca2+ signaling events that occur during the progression of the apoptotic cascade over a period of hours or days, has not yet been possible. Now using genetically encoded Ca2+ indicators complemented with automated epifluorescence microscopy we have shown that staurosporine‐induced apoptosis in MDA‐MB‐231 breast cancer cells was associated with delayed development of cytosolic free Ca2+ fluctuations, which were then maintained for 24 h. These cytosolic free Ca2+ fluctuations were dependent on the Ca2+ channel ORAI1. Silencing of ORAI1, but not its canonical activators STIM1 and STIM2, promoted apoptosis in this model. The pathway for this regulation implicates a mechanism previously associated with the migration of cancer cells involving ORAI1, the chaperone protein SigmaR1, and Ca2+‐activated K+ channels. | ||
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| 700 | 1 | |a Wood, Ian A. |4 aut | |
| 700 | 1 | |a Sadras, Francisco |4 aut | |
| 700 | 1 | |a Roberts‐Thomson, Sarah J. |4 aut | |
| 700 | 1 | |a Monteith, Gregory R. |4 aut | |
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