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. 2022 Oct 19;12:17440. doi: 10.1038/s41598-022-22156-6

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© The Author(s) 2022

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 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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Knockdown of claudin-3 in SVEC4-10 cell activated the PI3K signaling pathway. (a, b) Western blot analysis was conducted to detect the phosphorylation of AKT and ERK in transfected SVEC4-10 cells as indicated. Total AKT and ERK were detected for normalization. (**p < 0.01, ***p < 0.001) (n = 3 per group) (c) SVEC4-10 Control and OE cells were pretreated with the inhibitor of PI3K (LY294002) (10 μM) or ERK (PD98059) (10 μM). Scratching assay was conducted and the photos were taken under a microscope at the indicated time. Scale bar, 100 µm. (d) SVEC4-10 Control and knockdown cells (shClaudin-3) were pretreated with the inhibitor of PI3K (LY294002) (10 μM) or ERK (PD98059) (10 μM). Scratching assay was conducted and the photos were taken under a microscope at the indicated time. Scale bar, 500 µm. (e) Wound width of result in (c) was quantified and analyzed. (n.s.: no significance; ***p < 0.01) (n = 5 per group) (f) Wound width of result in (d) was quantified and analyzed. (n.s.: no significance; ***p < 0.01) (n = 5 per group).