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. 2018 Jan 8;8:37. doi: 10.1038/s41598-017-18280-3

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© The Author(s) 2017

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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(A) Bioinformatic analysis revealed an enrichment in DNMT1 sites on CASC9.5. (B) RNA immunoprecipitation assay showed that DNMT1 interacts with CASC9.5. (C) Bioinformatic analysis revealed that the CpG islands were present in the promoter region of E-cadherin. (D) Gene set enrichment analysis (GSEA) showed that CASC9.5 expression was related to tumor metastasis, tumor microenvironment and cyclin genes. (E) Western blot analysis of the expression status of cyclin D1, E-cadherin, N-cadherin and β-catenin in CASC9.5-knockdown (KD) A549 and SPC-A1 lung adenocarcinoma cell lines. (F) Immunofluorescence analysis of the expression of β-catenin in A549 lung adenocarcinoma cells after siRNA treatment. *p < 0.05, **p < 0.01.