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. 2022 Aug 16;21:163. doi: 10.1186/s12943-022-01634-5

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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. 3 — The targets and functions of METTL14 in gastrointestinal cancer. In liver cancer, METTL14 suppresses cancer development via downregulating EGFR, miR-126, SLC7A11 and upregulating USP48, HNF3γ, while promotes tumor progression via increasing SCD1 and ACLY expression. In GC, METTL14 suppresses cancer development via inhibiting circORC5, Wnt and PI3K/AKT/mTOR, while promotes tumor progression via upregulating Linc01320. In CRC, METTL14 suppresses cancer development via downregulating ARRDC4, SOX4, EBI3, STAT1/IRF1, LncRXIST and upregulating KLF4, miR-375, miR-149-3p, while promotes tumor progression via increasing PHLDB2 expression. In PC, METTL14 suppresses cancer development via downregulating PIK3CB, while promotes tumor progression via increasing CDA, AMPKα/ERK/mTOR, and downregulating PERP