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. 2023 Feb 1;12:985827. doi: 10.3389/fonc.2022.985827

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Copyright © 2023 Xu, Wang, Mo, Xie, Hu, Jiang, Hu, Ding and Xiao

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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CDK1 elevation partially reversed the inhibitory effects of NLE1 knockdown on non−small−cell lung cancer. (A) Celigo cell counting assay was employed to show the effects of alone overexpressing CDK1 as well as simultaneously downregulating NLE1 and overexpressing CDK1 on the cell proliferation of NCI-H1299 cells. (B) Colony formation assay was used to evaluate the abilities of NCI-H1299 cells to form colonies in CDK1 and CDK1+shNLE1 groups. (C, D) The migration abilities of NCI-H1299 cells were detected in CDK1 and CDK1+shNLE1 groups by transwell assay (C) and wound-healing assay (D). Magnification times: 200×. (E) The cell apoptosis of NCI-H1299 cells was examined by flow cytometry after infecting CDK1 and CDK1+shNLE1. Results were presented as mean ± SD (n ≥ 3). ** P < 0.01, *** P < 0.001, *P < 0.05.