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. 2017 May 18;7:2070. doi: 10.1038/s41598-017-02311-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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A model shows that the fragment HMGA2-sh-3p20 from HMGA2 mRNA 3′UTR promotes the growth of hepatoma cells by upregulating HMGA2. Bioinformatics analysis shows that 3′UTR of HMGA2 mRNA contains the hairpin structure (HMGA2-sh). Drosha and DGCR8 cleave the HMGA2-sh from the 3′UTR of HMGA2 mRNA, and Dicer contributes to the generation of the HMGA2-sh-3p20 from the HMGA2-sh. Furthermore, HMGA2-sh-3p20 is able to increase the levels of HMGA2 by antagonizing TTP-mediated HMGA2 degradation, while it decreases PTEN by targeting 3′UTR of PTEN mRNA. In addition, the downregulated-PTEN is not able to depress the expression of HMGA2, leading to the upregulation of HMGA2. Functionally, HMGA2-sh-3p20-enhanced HMGA2 accelerates the growth of liver cancer cells.