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. 2020 Aug 6;20:376. doi: 10.1186/s12935-020-01460-z

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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 — Knockdown of LINC00152 decreases the proliferation and invasion of lung cancer cells in vitro. a LINC00152 expression was analyzed by qRT-PCR in 5 NSCLC cell lines that were compared with the normal human bronchial epithelial cell line (16HBE). b, c LINC00152 mRNA levels in SPCA1 (b) and A549 (c) with LINC00152 siRNA (si-LINC00152) transfection compared with the negative control siRNA (NC) by qRT-PCR. d, e CCK-8 assays were performed to detect the viability of SPCA1 (d) and A549 (e) with LINC00152 siRNA transfection. f, g Transwell assays were performed to detect the invasion of SPCA1 (f) and A549 (g) with LINC00152 siRNA transfection. *: p < 0.05, **: p < 0.01, ***: p < 0.001