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. 2021 Feb 9;40:62. doi: 10.1186/s13046-021-01859-0

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© The Author(s) 2021

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. 7 — HOXA10 enhanced Smad2/3 expression in the cell nucleus and promoted the deposition of METTL3. a Western blot suggested that HOXA10 activated the Smad pathway but could be suppressed by TGFB2 inhibitor. b Confocal immunofluorescent staining indicated that HOXA10 promoted Smad2/3 translocation into the cell nucleus. c The colorimetric m⁶A assay demonstrated that HOXA10 elevated the m⁶A levels in GC cells. d Western blot showed that HOXA10 elevated METTL3 expression but could be repressed by TGFB2 inhibitor. e CoIP experiment revealed that Smad2/3 interacted with METTL3 in the nucleus of BGC823 cells. f ChIP-qPCR assay revealed the potential binding sites of Smad2/3 in the METTL3 promoter region. g Western blot showed that the protein expressions of P-Smad2/3 and METTL3 in AGS-HOXA10 cells were both reduced after being treated with ITD-1. Scale bars: 25 μm. ***P < 0.001