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. 2021 Mar 16;40:99. doi: 10.1186/s13046-021-01897-8

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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. 4 — YAP upregulates HMGB1 and promotes its translocation from nucleus to cytoplasm. a Heatmap showed the upregulated or downregulated proteins, which is associated with autophagy, after YAP over-expression in U87 glioma cells. b Representative immunoblots of the U87 and U251 cell extracts of the vector and YAP over-expression cells with indicated treatment probed with anti-YAP and anti-HMGB1 antibodies. c The mRNA level of HMGB1 after YAP over-expression both in U251 and U87 glioma cells. d Representative immunoblots of total lysates extracted from nontumor (n = 9) or different grade glioma tissues (n = 27) probed with indicated antibodies. e Quantitative analysis of the protein level of YAP and HMGB1 in gliomas. f The protein level of YAP and HMGB1 showed positive correlation in gliomas. r = 0.6938, p < 0.0001, n = 36. g Representative immunoblots of the extracts from tumors derived from vector and YAP over-expression cells without CQ treatment probed with indicated antibodies. h Subcellular location of HMGB1 was detected by using cellular fractionation. Histone and GAPDH were used as nucleus and cytoplasm loading control respectively. s.e: short exposure. l.e: long exposure. i Subcellular location of HMGB1 was assessed by immunofluorescence. Scale bar: 20 μm. *p < 0.05, **p < 0.01, ***p < 0.001