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. 2021 Aug 10;112(10):4176–4186. doi: 10.1111/cas.15089

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© 2021 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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The SMO agonist SAG reverses the effects of knocking down POU4F2 on CRC. A, Wound healing ability of HCT116 cells transfected with shNC or shPOU4F2‐1 and treated with SAG. B, Transwell assays showing the migration and invasion ability of HCT116 cells transfected with shNC or shPOU4F2‐1 and treated with SAG. C, Expression of the SHH, PTCH1, SMO, and GLI‐1 proteins in HCT116 cells transfected with shNC or shPOU4F2‐1 and treated with SAG. All experiments were performed in triplicate. Data are presented as the mean ± SEM (*P < .05, **P < .01, ***P < .001, ****P < .0001)