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. 2021 Aug 6;27:85. doi: 10.1186/s10020-021-00345-9

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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/.

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Fig. 5 — Silencing CASC18 inhibits CAL27 cell migration and invasion through repressing TGFB2-mediated EMT

A The silencing of CASC18 was conducted with the transfection of si-CASC18#1 and si-CASC18#2, as compared with si-NC. Representative photos of B wound healing and C assays indicate the role of CASC18 RNAi in cell migration and invasion. The right histograms denote the percentage of wound closure and the relative number of invaded cells, respectively. The impact of CASC18 knockdown on the D expressions of TGFB2, E-cadherin, N-cadherin, Vimentin by western blotting analysis with the reference of β-actin. E The mRNA levels of VIM and CDH1 genes were detected by qRT-PCR in two groups of clinical samples carrying high or low CASC18 expression. F The impact of CASC18 knockdown on the secretion of TGFB2 by ELISA. Data are presented as the mean ± SD. *p < 0.05