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. 2020 Dec 21;10:608300. doi: 10.3389/fonc.2020.608300

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Copyright © 2020 Hou, Jiang, Wang, Xie, Zhang, Feng, Ma, Ma, Liu and Hu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Atrx deficiency sensitizes NSCLC to ICI treatment in orthotopic mouse model. (A) experimental design for establishment of the orthotopic mouse model by intravenous seeding of tumor cells to analyze the tumor burden in vivo. (B) Kaplan-Meier survival curves of mice bearing LLC tumors with and without Atrx deficiency after anti-PD1 or anti-CTLA4 treatment. Neither aCTLA4 (n = 4) nor aPD1 (n = 4) treated mice showed a significant survival difference in Atrx-expression mice, compared with control group (n = 4) (P = 0.9341, 0.9412). Both aCTLA4 (n = 4) and aPD1 (n = 4) treated mice showed a significant survival difference in Atrx-deficient mice, compared with control group (n = 4) (P = 0.006, 0.003). (C) The luciferase signals detected by IVIS in mice bearing LLC generated tumors with and without Atrx deficiency after ICI or isotype antibody treatment. Neither aCTLA4 (n = 4) nor aPD1 (n = 4) treated mice showed a significant signal difference in Atrx-expression mice, compared with control group (n = 4) (P = 0.8521, 0.7644). Both aCTLA4 (n = 4) and aPD1 (n = 4) treated mice showed a significant signal difference in Atrx-deficient mice, compared with control group (n = 4) (P = 0.005, 0.002). **P<0.01. n.s., not significant.