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. 2015 Dec 15;14:208. doi: 10.1186/s12943-015-0480-4

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© Yu et al. 2015

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. 7 — A summary of the relationships between miR-214, UCP2, beclin-1, LC3-II, Bax, Caspase-9, PARP, and PI3K-Akt-mTOR after TAM/FUL treatment. TAM/FUL treatment results in autophagy as well as apoptosis. MiR-214 increased the sensitivity of breast cancer cells to the 4-OHT/FUL-induced apoptosis through inhibition of autophagy. UCP2 was identified to be a direct target of miR-214. Overexpression of UCP2 inhibited TAM/FUL-induced cell apotosis by increasing autophagy possibly through activation of the PI3K-Akt-mTOR signaling pathway, thereby contributing to endocrine resistance