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. 2022 Nov 16;41:323. doi: 10.1186/s13046-022-02526-8

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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. 6 — Overexpression of IFI16 or HuR reactivated the STAT3 and NF-κB signaling pathways in sh-ARPC1B GSCs. A Western blotting analysis of protein expression of ARPC1B, IFI16, HuR, P65, p-P65, STAT3, p-STAT3 and CD44 in GSC 20 cells treated with the indicated interventions. B The quantification of tumor sphere formation of GSC 267 and GSC 20 cells treated with the indicated interventions. C Limiting dilution assays of GSC 267 and GSC 20 cells treated with the indicated interventions. D Quantification of the apoptosis rates of GSC 267 and GSC 20 cells treated with the indicated interventions. E Quantification of DNA damage evaluated by the comet assay in GSC 267 and GSC 20 cells treated with the indicated interventions