Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils

Abstract Relatlimab and nivolumab combination therapy shows significant efficacy in treating various types of cancer. Current research on the molecular mechanisms of this treatment is abundant, but in-depth investigations into post-treatment resistance remain notably lacking. In this study, we ident...

Full description

Saved in:
Bibliographic Details
Main Authors: Xiaochen Wang, Maosheng Cheng, Shuang Chen, Caihua Zhang, Rongsong Ling, Shuqing Qiu, Ke Chen, Bin Zhou, Qiuli Li, Wenbin Lei, Demeng Chen
Format: Article
Language:English
Published: Nature Portfolio 2025-04-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59050-4
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849704310812704768
author Xiaochen Wang
Maosheng Cheng
Shuang Chen
Caihua Zhang
Rongsong Ling
Shuqing Qiu
Ke Chen
Bin Zhou
Qiuli Li
Wenbin Lei
Demeng Chen
author_facet Xiaochen Wang
Maosheng Cheng
Shuang Chen
Caihua Zhang
Rongsong Ling
Shuqing Qiu
Ke Chen
Bin Zhou
Qiuli Li
Wenbin Lei
Demeng Chen
author_sort Xiaochen Wang
collection DOAJ
description Abstract Relatlimab and nivolumab combination therapy shows significant efficacy in treating various types of cancer. Current research on the molecular mechanisms of this treatment is abundant, but in-depth investigations into post-treatment resistance remain notably lacking. In this study, we identify significant enrichment of SRY (sex determining region Y)-box 9 (Sox9)+ tumor cells in resistant samples using single cell RNA sequencing (scRNAseq) in a head and neck squamous cell carcinoma (HNSCC) mouse model. In addition, Sox9 directly regulates the expression of annexin A1 (Anxa1), mediating apoptosis of formyl peptide receptor 1 (Fpr1)+ neutrophils through the Anxa1-Fpr1 axis, which promotes mitochondrial fission, inhibits mitophagy by downregulating BCL2/adenovirus E1B interacting protein 3 (Bnip3) expression and ultimately prevents the accumulation of neutrophils in tumor tissues. The reduction of Fpr1+ neutrophils impairs the infiltration and tumor cell-killing ability of cytotoxic Cd8 T and γδT cells within the tumor microenvironment, thereby leading to the development of resistance to the combination therapy. We further validate these findings using various transgenic mouse models. Overall, this study comprehensively explains the mechanisms underlying resistance to the anti-LAG-3 plus anti-PD-1 combination therapy and identifies potential therapeutic targets to overcome this resistance.
format Article
id doaj-art-e64388235d5441279e6f1cd033812151
institution DOAJ
issn 2041-1723
language English
publishDate 2025-04-01
publisher Nature Portfolio
record_format Article
series Nature Communications
spelling doaj-art-e64388235d5441279e6f1cd0338121512025-08-20T03:16:47ZengNature PortfolioNature Communications2041-17232025-04-0116112010.1038/s41467-025-59050-4Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophilsXiaochen Wang0Maosheng Cheng1Shuang Chen2Caihua Zhang3Rongsong Ling4Shuqing Qiu5Ke Chen6Bin Zhou7Qiuli Li8Wenbin Lei9Demeng Chen10Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesDepartment of Head and Neck Surgery, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer CenterOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen UniversityAbstract Relatlimab and nivolumab combination therapy shows significant efficacy in treating various types of cancer. Current research on the molecular mechanisms of this treatment is abundant, but in-depth investigations into post-treatment resistance remain notably lacking. In this study, we identify significant enrichment of SRY (sex determining region Y)-box 9 (Sox9)+ tumor cells in resistant samples using single cell RNA sequencing (scRNAseq) in a head and neck squamous cell carcinoma (HNSCC) mouse model. In addition, Sox9 directly regulates the expression of annexin A1 (Anxa1), mediating apoptosis of formyl peptide receptor 1 (Fpr1)+ neutrophils through the Anxa1-Fpr1 axis, which promotes mitochondrial fission, inhibits mitophagy by downregulating BCL2/adenovirus E1B interacting protein 3 (Bnip3) expression and ultimately prevents the accumulation of neutrophils in tumor tissues. The reduction of Fpr1+ neutrophils impairs the infiltration and tumor cell-killing ability of cytotoxic Cd8 T and γδT cells within the tumor microenvironment, thereby leading to the development of resistance to the combination therapy. We further validate these findings using various transgenic mouse models. Overall, this study comprehensively explains the mechanisms underlying resistance to the anti-LAG-3 plus anti-PD-1 combination therapy and identifies potential therapeutic targets to overcome this resistance.https://doi.org/10.1038/s41467-025-59050-4
spellingShingle Xiaochen Wang
Maosheng Cheng
Shuang Chen
Caihua Zhang
Rongsong Ling
Shuqing Qiu
Ke Chen
Bin Zhou
Qiuli Li
Wenbin Lei
Demeng Chen
Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils
Nature Communications
title Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils
title_full Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils
title_fullStr Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils
title_full_unstemmed Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils
title_short Resistance to anti-LAG-3 plus anti-PD-1 therapy in head and neck cancer is mediated by Sox9+ tumor cells interaction with Fpr1+ neutrophils
title_sort resistance to anti lag 3 plus anti pd 1 therapy in head and neck cancer is mediated by sox9 tumor cells interaction with fpr1 neutrophils
url https://doi.org/10.1038/s41467-025-59050-4
work_keys_str_mv AT xiaochenwang resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT maoshengcheng resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT shuangchen resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT caihuazhang resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT rongsongling resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT shuqingqiu resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT kechen resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT binzhou resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT qiulili resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT wenbinlei resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils
AT demengchen resistancetoantilag3plusantipd1therapyinheadandneckcancerismediatedbysox9tumorcellsinteractionwithfpr1neutrophils