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. 2018 Feb 20;7(2):16. doi: 10.1038/s41389-018-0028-8

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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. 6 — a In situ hybridization (ISH) and immunohistochemistry analysis (IHC) of miR-214, ATG12, and LC3 in continuous sections of paraffin-embedded human CRC specimen. Bars represent 50 μm. Representative images were shown. b Correlations between miR-214 expression and ATG12 and LC3 in forty-two cases of human CRC tissues. c Schematic of miR-214 in the regulation of cell response to irradiation. Briefly, miR-214 inhibits cell autophagy by directly targeting ATG12. IR exposure enhances cell autophagy and inhibits apoptosis through downregulation of miR-214, thus causing IR resistance