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. 2022 Aug 19;41:252. doi: 10.1186/s13046-022-02467-2

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© The Author(s) 2022

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. 1 — Schematic illustration of PSPM-NPs and SLERCC in RCC progression. High DNMT3A was recruited at the SLERCC promoter, which induced aberrant hypermethylation, leading to downregulation of SLERCC expression in RCC. PSPM-NPs transfer SLERCC plasmids into cells by recognizing MUC12 molecules on the RCC cell membrane surface. Elevated SLERCC can directly interact with UPF1 to activate the Wnt/β-catenin signaling pathway, which in turn inhibits RCC metastasis and angiogenesis. Abbreviations: PSPM-NPs, Plasmid-SLERCC@PDA@MUC12 nanoparticles; RCC, Renal cell carcinoma