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. 2022 Sep 2;35(6):1912–1927. doi: 10.1007/s13577-022-00776-4

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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/.

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Fig. 3 — A The growth curve of HT-29 and HCT-116 cells transfected with non-siRNA, EGFR inhibitor, p-SPINK1 and SPINK1 siRNA (with/without EGFR inhibitor) cultured in 24 well plates during three days. B Wound healing assay and the percentage of migration cells of HT-29 and HCT-116 cells in 0 h, 24 h and 48 h after being treated with non-siRNA, EGFR inhibitor, p-SPINK1 and SPINK1 siRNA (with/without EGFR inhibitor). C Transwell invasion assay and the number of invaded cells of HT-29 and HCT-116 cell lines during a single day transfected treatment with non-siRNA, EGFR inhibitor, p-SPINK1 and SPINK1 siRNA (with/without EGFR inhibitor). The quantitative data analysis was expressed as mean ± SEM. *p < 0.05, **p < 0.01 and ***p < 0.001 as compared to the control group (n = 3/group); ^#p < 0.05, ^##p < 0.01 and ^###p < 0.001 as compared to the OV-SPINK1 group; ^§p < 0.05, ^§§p < 0.01§§ and ^§p < 0.001 as compared to the EGFRi group (n = 3/group)