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. 2021 Aug 6;19:232. doi: 10.1186/s12957-021-02339-7

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© The Author(s) 2021

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. 5 — C3G inhibited the proliferation, migration, and invasion, and promoted apoptosis in H1299 and A549 cells by downregulating TP53I3. A After the treatment of C3G (40 μM) or si-TP53I3, the cell clones of H1299 and A549 cells were determined by colony formation assay. B After the treatment of C3G (40 μM) or si-TP53I3, the apoptosis of H1299 and A549 cells was detected by flow cytometry. C After the treatment of C3G (40 μM) or si-TP53I3, the migration of H1299 and A549 cells was detected by transwell assay. D After the treatment of C3G (40 μM) or si-TP53I3, the invasion of H1299 and A549 cells was detected by transwell assay. ^**P < 0.01, vs. si-NC group; ^##P < 0.01, vs. si-TP53I3 group; ^&&P < 0.01, vs. C3G + si-NC group