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. 2018 Feb 14;9(2):233. doi: 10.1038/s41419-018-0275-9

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© The Author(s) 2018

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 Expression of FOXD2-AS1 in 19 pairs of TCGA cancer and adjacent noncancerous samples indicated that FOXD2-AS1 is obviously up-regulated in bladder cancer. b The location of FOXD2-AS1 on chromosome. c qRT-PCR performed in 84 cases showed that FOXD2-AS1 expression was significantly increased in bladder cacer tissues compared to adjacent noncancerous tissues (p < 0.01). d FOXD2-AS1 expression in MIBC patients was obviously higher than in NMIBC patients (p < 0.05). e Expression of FOXD2-AS1 was significantly higher in recurrence patients (p < 0.01). f Kaplan–Meier analysis revealed higher expression of FOXD2-AS1 is associated with poor prognosis. The p-values were assessed by log-rank test (p < 0.01). g Progression-free time was shorter in FOXD2-AS1 high expression patients. The p-values were assessed by log-rank test (p < 0.01). h ISH was performed in paraffin-embedded tissues. Expression of FOXD2-AS1 was extremely higher in relapsed tissues compared to adjacent noncancerous tissues and primary tumor tissues