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. 2021 Jan 7;40:20. doi: 10.1186/s13046-020-01807-4

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© The Author(s) 2020

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. 7 — Anti-GRP78 blockades exogenous GRP78-derived reinforcement of MES phenotype. a Western blotting for FLAG tag and total GRP78 in GSC20 transduced with vector control or WT FLAG-GRP78. b Nonpermeabilized Immunofluorescence staining of FLAG (red) in GSC20 transfected with FLAG-GRP78, taking vector as control. Scale bar, 10 μm, and 25 μm for the large field of view. c Western blotting for MES-related signatures CD44, YKL40 and pathways STAT3, p-STAT3, p65, p-p65 and C/EBPβ in GSC20 transfected with FLAG-GRP78 or vector control. d Western blotting for CD44, p65, p-p65 and C/EBPβ in GSC20 expressing FLAG-GRP78 with or without anti-GRP78 cotreatment for 48 h. e Flowcytometry demonstrated the apoptosis of GSC20 with 3 Gy radiation, which transfected with vector or FLAG-GRP78, with or without anti-GRP78 cotreatment. f Summary diagram for the possible mechanisms of csGRP78 playing an essential role in maintaining MES phenotype and targeting csGRP78 impairs BACE2 stabilization via lysosome-dependent degradation in MES subtype GSCs. Error bar indicates at least three independent experiments and data are shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001