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. 2023 Feb 23;23:33. doi: 10.1186/s12935-023-02874-1

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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. 7 — Circadian-hormone-KLF9 crosstalk in BCa. The KLF9 gene is coordinately regulated by GC (#1) and circadian (#2) signaling in normal breast epithelial cells. KLF9, in turn, feed backs to the breast circadian oscillator by modulating the GC (#3) and E2 (#4) response of core clock genes. In the context of BCa progression, KLF9 restricts oncogenesis in all mammary epithelial cell models used (#5). Moreover, in the luminal ER-expressing MCF7 cells, KLF9 enhanced the anti-tumorigenic effects of CORT signaling, while in triple-negative MCF10A and MDA-MB-231 cells, KLF9 restricted CORT-induced BCa progression