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. 2023 Jan 30;42:35. doi: 10.1186/s13046-022-02592-y

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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. 8 — Increased αSMA and LIF in the cancer stroma from obese and lean patients, respectively. A and C Formalin-fixed and paraffin-embedded (FFPE) T3/4 breast cancer tissue sections of lean (BMI ≤ 25) or obese (BMI ≥ 35) patients were immunohistochemically stained with LIF (C) or αSMA (A) antibody (brown), respectively, and counterstained with hematoxylin (blue). Scale: 100 μm. Inset I and II scale: 50 μm. B and D Quantification of the weighted score in breast cancer cells and tumor stroma for LIF (D) and αSMA (B). The results are presented as bar and scatter plots showing the mean value ± SEM (n = 32, 16 lean / 16 obese breast cancer tissues). Student’s t test was used. *p < 0.05, ***p < 0.001. E Table depicts LIF and αSMA staining intensity, percentage of positive tumor stroma and weighted score in 32 breast cancer tissue sections. F Schematic illustration of the proposed working model. The breast cancer TME has a crucial impact on the properties of bASCs and on their cell-cell interaction capacity. The de-differentiation process within the TME is highly dependent on the cellular context and is influenced by BMI of patients. Both cancer-educated bASCs phenotypes, iCAF and myCAF, have drastic impacts on breast cancer cells, leading to different tumor promoting profiles in low and high malignant cancer cells