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. 2022 Sep 28;13(9):835. doi: 10.1038/s41419-022-05238-1

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© The Author(s) 2022

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. 3 — A Scatter plot indicating the correlation of mRNA level of PTBP1, hnRNP A2/B1, and hnRNP K with ITSN1-S/ITSN1-L expression ratio using glioma RNA-Seq data from TCGA database. B Establishment and verification of stable cell lines underexpressing the 3 RBPs above. β-actin was used as an internal control. C Graphical representation of PCR primers for specific detection of ITSN1 and ITSN1-S, ITSN1-L isoforms. D RT–PCR detection of knockdown of the 3 RBPs above in LN229 cells on the expression levels of ITSN1, ITSN1-S, and ITSN1-L. E, F RT–qPCR analysis showing changes in the ITSN1-S, ITSN1-L, and total ITSN1 mRNA level (E) as well as the ratio of ITSN1-S/ITSN1-L (F) upon silencing of the 3 RBPs above in LN229 cells. Values were expressed as mean ± SD from six independent experiments in (E) and (F) (two-tailed Student’s t test, *P < 0.05, **P < 0.01, ***P < 0.001, ns, no significance).