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. 2017 Oct 30;36:151. doi: 10.1186/s13046-017-0626-x

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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. 3 — A schematic of the mechanism of synthetic regulatory RNAs. The mutant hTERT promoter drives the expression of aRNA. The amiRNA targeting MYC is driven by UAS. In HFF cells, aRNA cannot be expressed. The iRNA interacts with UAS so GAL4-VP64 cannot bind UAS to activate the expression of amiRNA. Artificial miRNAs can generate miRNAs that interact with the 3′ UTR of MYC mRNA completely and causes MYC mRNA degradation. However, aRNA is overexpressed in bladder cancer cells. The aRNA can interact with iRNA so UAS is exposed to GAL4-VP64 again. Thus, MYC amiRNA will be driven by the UAS and GAL4-VP64 complex