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. 2023 Jul 3;29:87. doi: 10.1186/s10020-023-00673-y

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — ORAI but not TRPC3 inhibition reduces NNAT-mediated elevation in intracellular Ca²⁺concentration in breast cancer cells. The overexpression of NNAT promotes significantly higher Ca²⁺ release from EndoR of ZR75 breast cancer cells. (n = 30 per group; paired t-test, ***p < 0.001 vs. control GFP) (A). Intracellular Ca²⁺ levels in standard and overexpressing NNAT T47D and ZR75 cell lines in the presence or absence of ORAI (pyr6) (B) or TRPC3 (pyr3) (C) pyrazole compound inhibitors (n = 30 per group; Two-way ANOVA tests (factors: NNAT and inhibitor; Tukey post hoc test) ***p < 0.001)