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. 2022 Feb 2;13(2):95. doi: 10.1038/s41419-022-04536-y

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© The Author(s) 2022

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A The activation of the WNT/β-catenin signaling was detected using a TOP/FOP flash assay. Proliferative abilities of oeVec plus si-NC, oeRBM5-AS1 plus si-NC, or oeRBM5-AS1 plus si-β-catenin transfected MCF-7 and MDA-MB-231 cells were evaluated by CCK-8 assays (B), plate colony assays (C, Scale bar, 1 cm), and EdU assays (D and E, Scale bar, 100 μm). F mRNA levels of pluripotent transcription factors in oeVec plus si-NC, oeRBM5-AS1 plus si-NC, or oeRBM5-AS1 plus si-β-catenin transfected MCF-7 and MDA-MB-231 cells. G Proportion of CD44+CD24− cells in oeVec plus si-NC, oeRBM5-AS1 plus si-NC, or oeRBM5-AS1 plus si-β-catenin transfected MCF-7 and MDA-MB-231 cells. H Sphere-formation abilities of oeVec plus si-NC, oeRBM5-AS1 plus si-NC, or oeRBM5-AS1 plus si-β-catenin transfected MCF-7 and MDA-MB-231 cells. Scale bar, 200 μm. I During breast tumorigenesis, RBM5-AS1 was upregulated by a hypoxia-induced transcriptional factor, RUNX2. RBM5-AS1 promoted proliferation, stemness, migration, and invasion of breast cancer cells via activating the WNT/β-catenin pathway in two ways. On the one hand, RBM5-AS1 could prevent β-catenin degradation by repressing transcription of AXIN1, a core component of the β-catenin destruction complex, which in turn facilitated β-catenin nucleus accumulation. On the other hand, RBM5-AS1 could function as a scaffold for β-catenin-TCF4 complex, leading to transcriptional activation of WNT/β-catenin signaling. All data are shown as the mean ± SEM. *P < 0.05 and **P < 0.01 by two-tailed Student’s t-test.