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. 2020 Aug 12;20:213. doi: 10.1186/s12890-020-01240-5

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© The Author(s) 2020

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — PCGEM1 is highly expressed in NSCLC cells and knockdown of it suppresses cell growth. a qRT-PCR was utilized to test the expression of PCGEM1 in NSCLC cell lines (A549, PC-9, NCI-H1299 and NCI-H1650) and the human lung bronchial epithelial cell line (BEAS-2B). b The interference efficiency of PCGEM1 in NCI-H1299 and NCI-H1650 cells was tested through qRT-PCR. c, d EdU and CCK-8 experiments were utilized to measure the cell proliferation when PCGEM1 was inhibited in NCI-H1299 and NCI-H1650 cells. e Flow cytometry analysis was implemented to evaluate cell apoptosis after PCGEM1 was knocked down in NCI-H1299 and NCI-H1650 cells. f, g Transwell assays were conducted to test cell migration and invasion after silencing of PCGEM1 in NCI-H1299 and NCI-H1650 cells. ^*P < 0.05, ^**P < 0.01