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. 2024 Nov 4;15:1463258. doi: 10.3389/fimmu.2024.1463258

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Copyright © 2024 Wu, Liu, Zeng, Ruan, Tao, Lin, Liu, Chen, Liu and Wu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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CTSK knockdown inhibits cell motility and migration. (A) A Transwell assay revealed reduced cellular mobility in CTSK-knockdown KTC-1 and cal-62 cells compared to control cells, demonstrating a significant reduction in the ability of these cells to traverse membrane pores. (B) Wound healing assays at 24 hours postwound creation revealed decreased motility in CTSK-knockdown KTC-1 and CTSK-knockdown cal-62 cells compared with that in the siNC group, as indicated by decreased closure rates. (C) Western blot analysis showing decreased levels of EMT markers, including Vimentin, N-cadherin, Snail, and Slug, in KTC-1 and CAL-62 cells following CTSK knockdown, with GAPDH serving as the loading control. The reduction in these proteins underscores significant suppression of EMT progression. ***P<0.001. Scale bar =100 μm.