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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. 4 — circLONP2 is essential for CRC metastasis. a, b Overexpression of circLONP2 significantly enhanced the migration and invasion ability of CRC cells. c, d Knockdown of circLONP2 by ASO significantly suppressed the migration and invasion ability of CRC cells. e, f In vivo tail vein injection model confirmed that overexpression or knockdown of circLONP2 could significantly promote or attenuate CRC cells metastasize to lung, respectively. All detection of circLONP2 by RT-qPCR was normalized to GAPDH. 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 Mann-Whitney U test (a, c, e, f), or independent Student’s t test (b, d)