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. 2021 May 19;7:117. doi: 10.1038/s41420-021-00498-w

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© The Author(s) 2021

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A, C Wound healing experiments were carried out to estimate the effects of SRSF1 on the migration in HepG2 and HCCLM3. B, D Wound healing experiments were carried out to estimate the effects of SRSF1 on the migration in HCCLM3. The magnification of Wound healing experiments is 100× and the scale length is 100 μm. E–H The effect of SRSF1, SRA1-L, and SRA1-S expression levels on the invasive ability of HepG2 cells was examined by trans-well assays. The magnification of trans-well assays is 200× and the scale length is 50 μm. Data are presented as mean ± S.D. (N = 3). The “*, **, ***” indicate “P < 0.05, 0.01, 0.001” versus the control group, respectively.