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. 2021 May 29;21:636. doi: 10.1186/s12885-021-08370-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 — RNAseq and gene set enrichment analysis (GHSEA) results for PGAP3-SRPK1 fusion knockdown. A) qPCR of MD8788–6 treated with PGAP3-SRPK1 siRNA compared to NT siRNA. Results are quantified as log2 fold change of NT siRNA samples. Results demonstrate knockdown of PGAP3/SRPK1 mRNA without changes in WT SRPK1 expression and confirm RNAseq results showing decreases in HSDL2 and CCDN1 and a small increase in FOXO4 with PGAP3-SRPK1 knockdown (n = 2 replicates). B) GSEA results demonstrating a negative correlation with KOBAYASHI_EGFR_SIGNALING_24HR_DN, HALLMARK_E2F_TARGETS, and HALLMARK_MYC_TARGETS_V1 pathways in samples with PGAP3-SRPK1 knockdown