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. 2021 Oct 13;21:535. doi: 10.1186/s12935-021-02226-x

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© The Author(s) 2021

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. 5 — Upregulation of EFNA3 in lung adenocarcinoma (LUAD) tissues and its relationship with clinicopathological features and outcomes. A Representative images of EFNA3 staining in LUAD tissue and paired normal lung tissue; B The IHC score of EFNA3 was significantly increased in LUAD tissues; EFNA3 staining score increased significantly with tumor size (C), lymph node metastasis (D) and advanced TNM stages (E); F Kaplan–Meier survival analysis and log-rank tests showed that high expression levels of EFNA3 were associated with poor prognosis (P = 0.001)