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. 2020 Oct 30;6:58. doi: 10.1038/s41523-020-00200-w

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a, b The half-life of CDK1 transcript was increased after RBM7 overexpression in SUM-1315 (a) and MCF-7 (b) cells. The control (NC) and RBM7 overexpression (RBM7) cells were treated with 5 µg/ml Act D for 0, 2, 4, 6, 8, 10, 12, and 14 h. c, d The half-life of CDK1 transcript was decreased after RBM7 knockdown in SUM-1315 (c) and MCF-7 (d) cells. The control (SCR) and RBM7 knockdown (Sh-1) cells were treated with 5 µg/ml Act D for 0, 2, 4, 6, 8, 10, 12, and 14 h. The relative quantification was calculated by the 2^−ΔΔCt method and normalized based on β-actin. e, f SUM-1315 and g, h MCF-7 cell lysates were immunoprecipitated with RBM7 antibody. PCR (e, g) and RT-qPCR (f, h) measured transcript levels of CDK1 and β-actin within RBM7 or IgG immunocomplexes in MCF-7 and SUM-1315 cell lysates (*P < 0.05). i Schematic diagram of various regions in the 3′-UTR of CDK1 mRNA. j, k The reporter containing CDK1 3′-UTR-B, C was increased by overexpression of RBM7 in SUM-1315 (j) and MCF-7 (k) cells. Data were shown as mean ± SD (*P < 0.05).