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. 2018 Apr 27;37:89. doi: 10.1186/s13046-018-0764-9

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© The Author(s). 2018

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 — Proposed working model of hypoxia-EZH2/miR-93-TGFBR2 axis in prostate cancer progression. Prostate cancer generates a hypoxic microenvironment which induces the expression of a series of downstream genes such as HIF-1α, HIF-1β, and TET1, which further promotes the upregulation of epigenetic modulator EZH2 and hypoxia-responsive miR-93. EZH2 may catalyze H3K27me3 or recruit several DNA methyltransferases, which results in higher level of promoter methylation of TGFBR2 gene and subsequent epigenetic silencing of TGFBR2. Besides, miR-93 may reduce the expression of TGFBR2 via binding to 3’-UTR of TGFBR2 mRNA, which can further repress the expression of TGFBR2