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. 2019 Dec 10;39(10):2212–2223. doi: 10.1038/s41388-019-1137-3

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© The Author(s) 2019

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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Fig. 1 — a Analysis of KPNA copy number alteration (CNA) in HNSCC from TCGA (http://cancergenome.nih.gov/). b Summary of KPNA4 amplification across different tumor types from TCGA. SA stomach adenocarcinoma, LA lung adenocarcinoma, CA colon adenocarcinoma, BIA breast invasive adenocarcinoma, LHC liver hepatocellular carcinoma, GM glioblastoma multiform, AML acute myeloid leukemia, SC sarcoma. c The expression of KPNA family transcripts in HNSCC from TCGA. d The expression of KPNA4 in nontumor tissue, and HNSCC samples from Cancer RNA-Seq Nexus (http://syslab4.nchu.edu.tw/). SI, SII, SIII, SIV denote stages I, II, III and IV. e KPNA4 mRNA expression across different types of cancer cells from CCLE (http://portals.broadinstitute.org/ccle/). f High KPNA4 expression (mRNA expression z-Scores (RNA-Seq V2 RSEM) >mean +2.0SD) was associated with poor disease-free survival of HNSCC patients in the TCGA cohorts.