Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer

Abstract Background Exposomes are critical drivers of carcinogenesis. However, how they modulate tumor behavior remains unclear. Extensive clinical data show cigarette smoke to be a key exposome that promotes aggressive tumors, higher rates of metastasis, reduced response to chemoradiotherapy, and s...

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Main Authors: Yang Li, Pedram Yadollahi, Fonma N. Essien, Vasanta Putluri, Chandra Shekar R. Ambati, Karthik Reddy Kami Reddy, Abu Hena Mostafa Kamal, Nagireddy Putluri, Lama M. Abdurrahman, Maria E. Ruiz Echartea, Keenan J. Ernste, Akshar J. Trivedi, Jonathan Vazquez-Perez, William H. Hudson, William K. Decker, Rutulkumar Patel, Abdullah. A. Osman, Farrah Kheradmand, Stephen Y. Lai, Jeffrey N. Myers, Heath D. Skinner, Cristian Coarfa, Kwangwon Lee, Antrix Jain, Anna Malovannaya, Mitchell J. Frederick, Vlad C. Sandulache
Format: Article
Language:English
Published: BMC 2025-04-01
Series:Journal of Translational Medicine
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Online Access:https://doi.org/10.1186/s12967-025-06258-z
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author Yang Li
Pedram Yadollahi
Fonma N. Essien
Vasanta Putluri
Chandra Shekar R. Ambati
Karthik Reddy Kami Reddy
Abu Hena Mostafa Kamal
Nagireddy Putluri
Lama M. Abdurrahman
Maria E. Ruiz Echartea
Keenan J. Ernste
Akshar J. Trivedi
Jonathan Vazquez-Perez
William H. Hudson
William K. Decker
Rutulkumar Patel
Abdullah. A. Osman
Farrah Kheradmand
Stephen Y. Lai
Jeffrey N. Myers
Heath D. Skinner
Cristian Coarfa
Kwangwon Lee
Antrix Jain
Anna Malovannaya
Mitchell J. Frederick
Vlad C. Sandulache
author_facet Yang Li
Pedram Yadollahi
Fonma N. Essien
Vasanta Putluri
Chandra Shekar R. Ambati
Karthik Reddy Kami Reddy
Abu Hena Mostafa Kamal
Nagireddy Putluri
Lama M. Abdurrahman
Maria E. Ruiz Echartea
Keenan J. Ernste
Akshar J. Trivedi
Jonathan Vazquez-Perez
William H. Hudson
William K. Decker
Rutulkumar Patel
Abdullah. A. Osman
Farrah Kheradmand
Stephen Y. Lai
Jeffrey N. Myers
Heath D. Skinner
Cristian Coarfa
Kwangwon Lee
Antrix Jain
Anna Malovannaya
Mitchell J. Frederick
Vlad C. Sandulache
author_sort Yang Li
collection DOAJ
description Abstract Background Exposomes are critical drivers of carcinogenesis. However, how they modulate tumor behavior remains unclear. Extensive clinical data show cigarette smoke to be a key exposome that promotes aggressive tumors, higher rates of metastasis, reduced response to chemoradiotherapy, and suppressed anti-tumor immunity. We sought to determine whether smoke itself can modulate aggressive tumor behavior in head and neck squamous cell carcinoma (HNSCC) through reprogramming of the cellular reductive state. Methods Using established human and murine HNSCC cell lines and syngeneic mouse models, we utilized conventional western blotting, steady state and flux metabolomics, RNA sequencing, quantitative proteomics and flow cytometry to analyze the impact of smoke exposure on HNSCC tumor biology and anti-tumor immunity. Results Cigarette smoke persistently activated Nrf2 target genes essential for maintenance of the cellular reductive state and survival under conditions of increased oxidative stress in HNSCC regardless of human papillomavirus (HPV) association. In contrast to e-cigarette vapor, conventional cigarette smoke mobilizes cellular metabolism toward oxidative stress adaptation, resulting in development of cross-resistance to cisplatin. In parallel, smoke exposure modulates expression of PDL1 and the secretory phenotype of HNSCC cells resulting in an altered tumor immune microenvironment (TIME) in syngeneic mouse models and downregulated expression of antigen presentation and costimulatory genes in myeloid cells. Conclusion The cigarette smoke exposome is a potent activator of the Nrf2 pathway and appears to be the primary trigger for a tripartite phenotype of aggressive HNSCC consisting of: (1) reduced chemotherapy sensitivity, (2) enhanced metastatic potential and (3) suppressed anti-tumor immunity.
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spelling doaj-art-aa686be31fce4dfc97f22f664eb196db2025-08-20T03:07:44ZengBMCJournal of Translational Medicine1479-58762025-04-0123112110.1186/s12967-025-06258-zTobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancerYang Li0Pedram Yadollahi1Fonma N. Essien2Vasanta Putluri3Chandra Shekar R. Ambati4Karthik Reddy Kami Reddy5Abu Hena Mostafa Kamal6Nagireddy Putluri7Lama M. Abdurrahman8Maria E. Ruiz Echartea9Keenan J. Ernste10Akshar J. Trivedi11Jonathan Vazquez-Perez12William H. Hudson13William K. Decker14Rutulkumar Patel15Abdullah. A. Osman16Farrah Kheradmand17Stephen Y. Lai18Jeffrey N. Myers19Heath D. Skinner20Cristian Coarfa21Kwangwon Lee22Antrix Jain23Anna Malovannaya24Mitchell J. Frederick25Vlad C. Sandulache26Bobby R. Alford Department of Otolaryngology Head and Neck Surgery, Baylor College of MedicineBobby R. Alford Department of Otolaryngology Head and Neck Surgery, Baylor College of MedicineBobby R. Alford Department of Otolaryngology Head and Neck Surgery, Baylor College of MedicineAdvanced Technology Cores, Dan Duncan Cancer Center, Baylor College of MedicineAdvanced Technology Cores, Dan Duncan Cancer Center, Baylor College of MedicineAdvanced Technology Cores, Dan Duncan Cancer Center, Baylor College of MedicineAdvanced Technology Cores, Dan Duncan Cancer Center, Baylor College of MedicineAdvanced Technology Cores, Dan Duncan Cancer Center, Baylor College of MedicineBobby R. Alford Department of Otolaryngology Head and Neck Surgery, Baylor College of MedicineDan L Duncan Comprehensive Cancer Center, Baylor College of MedicineDepartment of Pathology and Immunology, Baylor College of MedicineDepartment of Pathology and Immunology, Baylor College of MedicineDepartment of Pathology and Immunology, Baylor College of MedicineDan L Duncan Comprehensive Cancer Center, Baylor College of MedicineDan L Duncan Comprehensive Cancer Center, Baylor College of MedicineDepartment of Radiation Oncology, Baylor College of MedicineDepartment of Head and Neck Surgery, University of Texas MD Anderson Cancer CenterDepartment of Medicine-Pulmonary, Baylor College of MedicineDepartment of Head and Neck Surgery, University of Texas MD Anderson Cancer CenterDepartment of Head and Neck Surgery, University of Texas MD Anderson Cancer CenterDepartment of Radiation Oncology, University of PittsburghDan L Duncan Comprehensive Cancer Center, Baylor College of MedicineMass Spectrometry Proteomics Core, Baylor College of MedicineMass Spectrometry Proteomics Core, Baylor College of MedicineVerna and Marrs Mclean Department of Biochemistry and Molecular Pharmacology, Baylor College of MedicineBobby R. Alford Department of Otolaryngology Head and Neck Surgery, Baylor College of MedicineBobby R. Alford Department of Otolaryngology Head and Neck Surgery, Baylor College of MedicineAbstract Background Exposomes are critical drivers of carcinogenesis. However, how they modulate tumor behavior remains unclear. Extensive clinical data show cigarette smoke to be a key exposome that promotes aggressive tumors, higher rates of metastasis, reduced response to chemoradiotherapy, and suppressed anti-tumor immunity. We sought to determine whether smoke itself can modulate aggressive tumor behavior in head and neck squamous cell carcinoma (HNSCC) through reprogramming of the cellular reductive state. Methods Using established human and murine HNSCC cell lines and syngeneic mouse models, we utilized conventional western blotting, steady state and flux metabolomics, RNA sequencing, quantitative proteomics and flow cytometry to analyze the impact of smoke exposure on HNSCC tumor biology and anti-tumor immunity. Results Cigarette smoke persistently activated Nrf2 target genes essential for maintenance of the cellular reductive state and survival under conditions of increased oxidative stress in HNSCC regardless of human papillomavirus (HPV) association. In contrast to e-cigarette vapor, conventional cigarette smoke mobilizes cellular metabolism toward oxidative stress adaptation, resulting in development of cross-resistance to cisplatin. In parallel, smoke exposure modulates expression of PDL1 and the secretory phenotype of HNSCC cells resulting in an altered tumor immune microenvironment (TIME) in syngeneic mouse models and downregulated expression of antigen presentation and costimulatory genes in myeloid cells. Conclusion The cigarette smoke exposome is a potent activator of the Nrf2 pathway and appears to be the primary trigger for a tripartite phenotype of aggressive HNSCC consisting of: (1) reduced chemotherapy sensitivity, (2) enhanced metastatic potential and (3) suppressed anti-tumor immunity.https://doi.org/10.1186/s12967-025-06258-zTobaccoNrf2Oxidative stressKeap1GlutathionePDL1
spellingShingle Yang Li
Pedram Yadollahi
Fonma N. Essien
Vasanta Putluri
Chandra Shekar R. Ambati
Karthik Reddy Kami Reddy
Abu Hena Mostafa Kamal
Nagireddy Putluri
Lama M. Abdurrahman
Maria E. Ruiz Echartea
Keenan J. Ernste
Akshar J. Trivedi
Jonathan Vazquez-Perez
William H. Hudson
William K. Decker
Rutulkumar Patel
Abdullah. A. Osman
Farrah Kheradmand
Stephen Y. Lai
Jeffrey N. Myers
Heath D. Skinner
Cristian Coarfa
Kwangwon Lee
Antrix Jain
Anna Malovannaya
Mitchell J. Frederick
Vlad C. Sandulache
Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
Journal of Translational Medicine
Tobacco
Nrf2
Oxidative stress
Keap1
Glutathione
PDL1
title Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
title_full Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
title_fullStr Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
title_full_unstemmed Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
title_short Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
title_sort tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer
topic Tobacco
Nrf2
Oxidative stress
Keap1
Glutathione
PDL1
url https://doi.org/10.1186/s12967-025-06258-z
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