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. 2022 Jul 15;21:146. doi: 10.1186/s12943-022-01607-8

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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. 6 — CircPOLR2A exerted its biological functions by inhibiting PEBP1 expression in cRCC cells. a, b Cell apoptosis was determined after cell transfection. 6a, 786O cells; 6b, Caki1 cells. c, f Transwell assay in rescue experiments. 6c, the effect of circPOLR2A knockdown in 786O cells could be counteracted by PEBP1 inhibition; 6f, the role of circPOLR2A overexpression in Caki1 cells could be rescued by PEBP1 overexpression. Scale bar, 40 μm. d, g Wound healing assay for rescue experiments. Scale bar, 100 μm. e, h Statistical analysis of the cell migration and invasion assays