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. 2023 Mar 30;22:65. doi: 10.1186/s12943-023-01765-3

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© The Author(s) 2023

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — HOTAIR inhibits tumor suppressor miRNAs and activates pro-oncogenic miRNAs in BC. Activation of oncogenic miRNAs enhances the expression of EMT-specific proteins involved in metastasis by activating HOTAIR expression. HOTAIR regulates the miR-129-5p/FZD7 axis, which promotes EMT via the regulation of E-cadherin and N-cadherin vimentin. HOTAIR also activates the miR601/ZEB1 axis, which promotes metastasis by activating AKT. HOTAIR promotes angiogenesis by inducing the transcription of VEGF via direct interaction at the promoter or the activation of the GRP78/Ang2 axis