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. 2015 Sep 28;1:15001. doi: 10.1038/npjsba.2015.1

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Copyright © 2015 The Systems Biology Institute/Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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MiR-365a-3p regulates chromatin modifiers and is associated with poor outcome of cancer patients. (a) Gene ontology-based analysis of mRNA targets of miR-365a-3p. These are predicted mRNA targets with evidence of binding by the argonaute from AGO-CLIP-seq data from multiple cell lines. (b) Network of predicted and validated targets of miR-365a-3p. (c) Heat map of the fold change in expression of genes in b after transfection of SKOV3.ip1 and MDA-MB-231 cell lines with miR-365a-3p. (d) Increased histone H3 acetylation of lysine 9 in cell lines after miR-365a-3p transfection. (e) Kaplan–Meier plots of the overall survival of The Cancer Genome Atlas (TCGA) patients with several different cancers grouped according to miR-365a-3p expression. (f) Box–whisker plot of the results of the growth of xenograft human tumor cells (SKOV3.ip1) grafted into mice and treated with anti-miR-365a-3p incorporated into dioleoylphosphatidylcholine (DOPC) nanoliposomes.