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. 2023 Aug 21;42:215. doi: 10.1186/s13046-023-02777-z

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© The Author(s) 2023

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 — METTL1 regulates CRPC proliferation and invasion by modulating the expression of CDK14. A Validation of CDK14 expression in TMA containing HSPC and CRPC tissues using IHC assay. Objective magnification: 40X, 100X, and 200X. B The proportion of patients with different CDK14 levels according to the IHC staining result. C The different mRNA expressions of CDK14 between HSPC and CRPC cell lines by RT-qPCR. D-F RT-qPCR and western blot were performed to detect the CDK14 level after METTL1 was rescued and inhibition of CDK14 using siRNA or not. G-I Proliferation ability of LNCaP-AI and C4-2 were assessed through MTT and colony formation experiments after METTL1 was rescued and CDK14 was suppressed. J Invasion capacity of LNCaP-AI and C4-2 were evaluated via transwell experiments after METTL1 was rescued and CDK14 was suppressed. **P < 0.01; ****P < 0.0001