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. 2017 Dec 7;17:832. doi: 10.1186/s12885-017-3827-y

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 6 — Signaling axis mediated by PKCα enhances cellular migration and invasion. In cells without PKCα expression (left), p120-catenin binds to the cytoplasmic domain of E-cadherin and stabilizes the AJs. In endocrine resistant ER⁺ breast cancer and basal A TNBC (right), PKCα increases FOXC2 expression and promotes its repression of p120-catenin transcription. As a result, E-cadherin is destabilized and prone to degradation, leading to dissociation of the AJ and intercellular connections