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. 2018 Oct 19;9(11):1068. doi: 10.1038/s41419-018-1088-6

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© The Author(s) 2018

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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Fig. 3 — a MiR4673 can hybridise to cdk-18 with high affinity (left). Application of miR4673 inhibited cdk-18 in a dose-dependent manner. E1, E2, E3 are sequential electroporations 24 h apart (** indicates p < 0.01). b Ultrastructural changes of SKBR3 cells after amplification of the endogenous miRNA (Red: nucleus & Aqua: mitochondria). Note stabilised actin microfilaments (middle) and autophagy (black arrow) subsequent to amplification of the endogenous miRNA. The observed ultrastructural changes following amplification of miR4673 contrast sharply with the numerous active perinuclear mitochondria detected after application of Paclitaxel (right). Amplification of miR4673 signalling triggered mitophagy (bottom, blue arrowhead) in contrast to Paclitaxel-induced activation of mitochondria (bottom right, orange arrowhead) Insets show mitochondrial ultrastructure (scale bars: top = 2 μm, middle left = 0.5 μm, middle = 0.7 μm, middle right = 1 μm, bottom left, bottom left = 0.2 μm, bottom middle = 0.6 μm, bottom right = 0.3 μm, bottom left)