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. 2022 Nov 17;17:33. doi: 10.1186/s13062-022-00347-5

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© The Author(s) 2022

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 — SH3BP5-AS1 was upregulated in GEM-treated PDX pancreatic cancer and its upregulation was negatively correlated with overall survival. A Establishment of the PDX pancreatic cancer model and experimental workflow of GEM treatment. B Heatmap displaying the top 10 upregulated lncRNAs in GEM-treated and control PDX mice. C Correlation analysis of SH3BP5-AS1 and clinicopathological features based on the TCGA database. D SH3BP5-AS1 was upregulated in pancreatic cancer tumor tissues compared with the paired adjacent tissues, as revealed by RT-qPCR. E SH3BP5-AS1 is an independent risk factor for the prognosis of pancreatic cancer, as revealed by ROC curve analysis. F Upregulation of SH3BP5-AS1 was correlated with poor overall survival. G SH3BP5-AS1 expression was significantly higher in pancreatic cancer cells compared with HPDE6-C7 cells. Data are shown as the mean ± SD. *P < 0.05; **P < 0.01