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. 2022 Feb 4;10(2):e003716. doi: 10.1136/jitc-2021-003716

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© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See https://creativecommons.org/licenses/by/4.0/.

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Schematic diagram showing the mechanism by which KDM4C is involved in antitumor immunity in lung cancer. Left panel: KDM4C is abnormally upregulated in lung cancer cells. By reducing the enrichment of the activated histone H3K36me3 at the promoter of CXCL10 and inhibiting CXCL10 expression, KDM4C reduces the infiltration and activation of CD8⁺ T cells, which converts the tumor to a ‘cold’ state that is insensitive to radiotherapy and immunotherapy. Right panel: targeted pharmacological inhibition of KDM4C using SD70 can reprogram the epigenetic state in a tumor, activate the expression of CXCL10, and enhance the recruitment and activation of CD8⁺ T cells, converting the tumor to a ‘hot’ state that is sensitive to radiotherapy and immunotherapy.