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. 2019 Feb 11;11(2):208. doi: 10.3390/cancers11020208

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Hypoxia-induced Orai3 up-regulation is HIF1α dependent. (A) The ORAI3 genomic region on human chromosome 16. Displayed are the histone modifications (human m epithelial cells, HMEC) indicative of active promoters, conservation (Phastcons), CpG islands, HIF1 binding (MCF7 cells) and HIF motifs. Confirmation of HIF1α (B) and HIF1β (C) siRNA-mediated silencing and the effect of HIF1α (D) and HIF1β (E) silencing (**** p < 0.0001, unpaired t-test) on the induction of ORAI3 by hypoxia in MDA-MB-468 cells. (F) Representative immunoblot and (G) densitometry analysis of the effect of ORAI3 silencing on hypoxia-mediated increases of HIF1α protein in MDA-MB-468 cells compared to NT siRNA in normoxia and hypoxia. ns = not significant (p ≥ 0.05), * p < 0.05, ** p < 0.01, *** p < 0.001 (one-way ANOVA, with Bonferroni’s multiple comparisons), n = 3, mean ± SD.