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. 2021 Oct 9;30(3):605–617. doi: 10.1038/s41418-021-00888-8

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© The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare 2021, corrected publication 2022Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 8 — A A549 cells with stable expression of shRMRP (A549/shRMRP) or scrambled control (A549/Scrambled) were transplanted into the axilla of nude mice to construct tumor growth model. Representative images of nude mice and tumors. B A549/Scrambled and A549/shRMRP group samples were collected and analyzed by qRT-PCR (n = 3). C Tumor volumes in the A549/Scrambled and A549/shRMRP groups. D Tumor weight in the A549/Scrambled and A549/shRMRP groups. E Representative images of haematoxylin and eosin (H&E) staining, Ki-67, MMP9, and TGFBR1 expression by immunohistochemical analysis in xenograft tumors derived from A549/Scrambled and A549/shRMRP groups. F Flowchart of our experiments. Our study suggests the m6A mark improved the stability of methylated RMRP transcripts by decreasing the RNA degradation rate, which may partially account for the upregulation of RMRP in NSCLC. Furthermore, RMRP promotes TGFBR1 transcription by recruiting YBX1 to TGFBR1 promoter.