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. 2022 Jan 11;13(1):51. doi: 10.1038/s41419-022-04500-w

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© The Author(s) 2022

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. 5 — A Venn diagram depicting 9 candidate common targets of miR-145-5p and linc01133. B The complementary sequence of YES1 3’UTR with miR-145-5p seed sequence predicted by TargetScan and the mutated sequence. MiR-145-5p reduced the luciferase activity of pmirGLO-YES1 3’UTR but not that with miR-145-5p binding site mutation in MKN45 (C) and HEK293 cells (D). MiR-145-5p inhibited YES1 expression in both mRNA (E)and protein level (F). G YES1 3’UTR is AGO2 bounded demonstrated by RIP assay. H YES1 could be pulled down by biotin-labeled miR-145-5p. Linc01133 overexpression in HGC27 cells or knocking-down in AGS cells increased or decreased the expression of YES1 both in mRNA (I, J) and protein level (K). L Linc01133 greatly attenuated miR-145-5p induced YES1 down-regulation. Each experiment was performed in triplicates. Data are shown as mean ± SD, *P < 0.05, **P < 0.01.