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. 2021 Jan 18;7:627774. doi: 10.3389/fmolb.2020.627774

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Copyright © 2021 Zhang, Chen, Zhu, Zhu, Liao, Wu, Cheng, Zhang, Mei and Yang.

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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Knockdown of GACAT3 induced cellular phenotypic changes via p21, Bax, and E-cadherin regulation. After transfection of CRISPR-Cas13, CCK-8 assay, wound healing assay, and ELISA assay were used to detect cell proliferation, migration and apoptosis, respectively. (A) p21 CRISPR-Cas13 eliminated the proliferation inhibition effects induced by GACAT3 CRISPR-Cas13 in T24 and 5637 (p < 0.05). (B) E-cadherin CRISPR-Cas13 eliminated the migration inhibition effects induced by GACAT3 CRISPR-Cas13 in T24 and 5637, whereas p21 CRISPR-Cas13 has no such function (***p < 0.001). (C) Bax CRISPR-Cas13 eliminated the apoptosis-promoting effects induced by GACAT3 CRISPR-Cas13 in T24 and 5637, whereas E-cadherin CRISPR-Cas13 has no such function (*p < 0.05).