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. 2023 Nov 3;20(1):25–51. doi: 10.1007/s12015-023-10647-6

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© The Author(s) 2023

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 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/.

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Fig. 3 — Mechanotransduction signaling mediated by integrin interaction with extracellular matrix (ECM) modulates CD133 expression in response to stiffness changes. The impact of ECM-cell interaction in CD133 levels can differ between traditional 2D (monolayer) and 3D in vitro models. A Monolayer cultures on stiffer matrices promote the establishment of focal adhesions that transduce mechanical forces in signaling activation, such as PI3K signaling. Also, contractile forces transmission to the nucleus can modulate pathways at the transcriptional level modulating transcription coactivators, transcription factors, and chromatin accessibility. By contrast, cells embedded in ECM sense mechanical clues such as stiffness via integrins, but the downstream signaling is unclear. B Soft matrices in 3D models increased CD133 expression through the improved expression of Sox2, Oct4, and regulation of chromatin accessibility to PROM1 promoter while repressing the expression of THBS2. CD133 in cell surface improves PI3K /Akt signaling, which can increase Sox2 and Nanog levels. Created with BioRender.com