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. 2021 Feb 1;40:52. doi: 10.1186/s13046-021-01857-2

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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. 8 — METTL3-Mediated modification of HMGA1 stabilized HMGA1 expression in CRC. a-b qRT-PCR and western blot assays showed the mRNA and protein expression, respectively, of HMGA1 in HCT116 and SW480 cells with METTL3 knockdown. Results was normalized with GAPDH (*p < 0.05). c-d qRT-PCR and western blot assays showed the mRNA and protein expression of HMGA1 in LINC00460 overexpression HCT116 and SW480 cells with METTL3 knockdown. Results was normalized with GAPDH (**p < 0.01, ***p < 0.001). e-f m⁶A immunoprecipitation and qRT-PCR assays showed the relative expression HMGA1 mRNA with methylation. Relative HMGA1 fold changes were normalized with the input, IgG was used as a negative control (*p < 0.05, **p < 0.01, ***p < 0.001)