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. 2022 Sep 23;20:426. doi: 10.1186/s12967-022-03633-y

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 2 — MIR99AHG targets miR-136-5p to exert its tumor suppressive effects in LUAD. A DIANA database analysis of LncRNA MIR99AHG binding sites to miR-136-5p. B Expression of MIR99AHG was examined by RT-qPCR after knocking down miR-136-5p. C Expression of miR-136-5p was examined by RT-qPCR after overexpression of MIR99AHG. D Putative binding sequence between MIR99AHG and miR-136-5p. E After transfection in HEK293T cells according to experimental subgroups, luciferase activity analysis (n = 3). F Luciferase reporters containing MIR99AHG-Luc-WT were co-transfected with or without miR-136-5p and MIR99AHG, Luciferase activity was determined using a dual luciferase reporter system. G FISH results show the colocalization of MIR99AHG and miR-136-5p in the cytoplasm of LUAD cells