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. 2020 May 8;18(2):1559325820923825. doi: 10.1177/1559325820923825

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© The Author(s) 2020

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — PRKCSH-2 deficiency promotes lung cancer cell proliferation. A, Representative image of lung A549 cells with or without TGFβ treatment (magnification, ×40). B, Cell Counting Kit-8 (CCK-8) assay was used to determine the effect of silencing the PRKCSH splice variants on the cell proliferation. C, Wound healing assay showed that silence of PRKCSH-2 significantly repressed cell migration ability of A549 cells (magnification, ×10). D, Quantitative determination of wounding healing results. The results represent the average of 3 independent experiments (mean ± standard error of the mean); *P < .05. E, Flow cytometric analysis of cell cycle in 5 groups, control group, TGFβ treatment, TGFβ treatment + negative control (NC), TGFβ treatment + siPRKCSH-1, and TGFβ treatment + siPRKCSH-2. F, Quantitative determination of wounding healing results. The results represent the average of 3 independent experiments (mean ± standard error of the mean); *P < .05.