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. 2024 Jun 7;19:44. doi: 10.1186/s13062-024-00486-x

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© The Author(s) 2024

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 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. 6 — METTL3 deficiency inhibited OS cell progression by altering MCAM expression. MG63 and U2OS cells were transfected with sh-NC, sh-METTL3, sh-METTL3 + pcDNA or sh-METTL3 + MCAM. (A) MCAM protein level in MG63 and U2OS cells was measured via western blot. (B) MG63 and U2OS cell viability was assessed by MTT assay. (C) The colony formation of MG63 and U2OS cells was estimated by colony formation assay. (D and E) The apoptosis of MG63 and U2OS cells was analyzed by flow cytometry analysis. (F and G) The invasion and migration of MG63 and U2OS cells were evaluated by transwell assay and wound-healing assay, respectively. (H and I) The protein levels of CyclinD1 and MMP9 in MG63 and U2OS cells were detected by western blot. *P < 0.05, **P < 0.01, ***P < 0.001