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. 2021 Oct 21;22(21):11366. doi: 10.3390/ijms222111366

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Ca²⁺-mediated phenotypic changes in CAFs. (A), TGFβ1-induced breast CAF differentiation is partially mediated by L and T-type VGCCs. (B), PDAC-conditioned media activate CAF TRPC3, and the Ca²⁺ influx promotes CAF migration. (C), CRC-secreted 12(S)-HETE activates the CAF BLT2 receptor and induces an increase in [Ca²⁺]_CYT. (D), Breast cancer-secreted estrogen activates CAF GPER, increasing [Ca²⁺]_CYT and promoting CAF migration and proliferation. (E), Irradiated glioma-conditioned media activate CAF L-type VGCCs, and the Ca²⁺ influx promotes genetic instability and micronuclei formation. (F), Breast CAFs can phagocytose breast cancer apoptotic bodies in a Ca²⁺-dependent manner; this promotes horizontal gene transfer and malignant transformation in CAFs.