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. 2020 Oct 9;11(10):836. doi: 10.1038/s41419-020-03049-w

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© The Author(s) 2020

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. 8 — a, b Cell viability assays of METTL3-overexpressing MKN-45 (lvM3), METTL3-reducing HGC-27 (shM3), and control (lvCTL and shCTL) cells, with (5 or 50 µg/mL) or without everolimus (E). c Tumor volume of mice carrying METTL3-high or control tumors and fed with everolimus or solvent. Mice were pre-inoculated with MKN-45 tumor cells, administrated with everolimus or solvent daily from day 0 to 16, then sacrificed at day 17. d Photos of xenograft tumors when mice were sacrificed. e Tumor inhibition rate of everolimus in METTL3-high and control tumors. Tumor inhibition rate = 1 − the tumor weight with everolimus/the corresponding tumor weight with solvent. f Overview of METTL3/m⁶A-mediated miRNA cluster biogenesis and AKT/mTOR pathway activation in gastric cancer development. n = 3 for each group. Data are presented as mean ± SD. *P < 0.05.