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. 2017 Jun 29;8(6):e2897. doi: 10.1038/cddis.2017.288

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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A possible mechanism of KDM2B regulation of apoptotic response in GBM cells. KDM2B modulates the H3K36 methylation levels of target proapoptotic genes to suppress their expression levels. RNAi-mediated knockdown or TRAIL-sensitizing agents downregulate KDM2B, which in turn lead to sensitization of GBM cells by increased transcription of proapoptotic genes. In accordance, silencing of HMTs responsible for the same histone modification confers GBM cells more resistant to TRAIL-induced apoptosis