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. 2020 Mar 18;19:60. doi: 10.1186/s12943-020-01184-8

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© The Author(s) 2020

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. 3 — The biogenesis of circLONP2 is regulated by FUS. a Different deletion mutants for circLONP2-overexpressing plasmid. b RT-qPCR showed that only the wild type could significantly and stably overexpress circLONP2, normalized to GAPDH. c Knockdown of FUS significantly decreased the expression of circLONP2, normalized to GAPDH. d anti-FUS RIP showed significant enrichment of both I7RCM and I11RCM. e The expression of FUS and circLONP2 in CRC tissue showed significant positive correlation, normalized to GAPDH. f The mRNA level of FUS were correlated with prognosis of CRC patients in TCGA database. All experiments were repeated for three times, data were shown as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 in one-way ANOVA (b, c), Mann-Whitney U test (d), person correlation test (e) or log-rank test (f)