Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer

Tobacco smoking is the major cause of non-small-cell-lung cancer (NSCLC). However, it is barely known how smoking impact the tumor immune environment (TIME) of lung cancer.We integrated single-cell RNA-seq and bulk RNA-seq data from several studies to systematically study the impact of smoking on T...

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Autores principales:	Yudi Hu, Chaoqun Xu, Jun Ren, Yuanyuan Zeng, Fengyang Cao, Hongkun Fang, Guo Jintao, Ying Zhou, Qiyuan Li
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2022
Materias:	Lung cancer Single cell Tumor immune microenvironment Smoking Treg Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/6d02312e5664443cb9997c267a2ba995
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spelling	oai:doaj.org-article:6d02312e5664443cb9997c267a2ba9952021-11-10T04:22:44ZExposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer1936-523310.1016/j.tranon.2021.101261https://doaj.org/article/6d02312e5664443cb9997c267a2ba9952022-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1936523321002527https://doaj.org/toc/1936-5233Tobacco smoking is the major cause of non-small-cell-lung cancer (NSCLC). However, it is barely known how smoking impact the tumor immune environment (TIME) of lung cancer.We integrated single-cell RNA-seq and bulk RNA-seq data from several studies to systematically study the impact of smoking on T cells in treatment naïve NSCLC patients. We defined a set of smoking-induced differentially expressed genes (SIDEGs) in different cells in TIME.. Specifically, we defined a smoking-related tumor-specific Treg subset, ADAM12+ CTLA4+ Tregs according to the trajectory analysis and highly express genes in cell adhesion pathways and lipid metabolism. Using independent datasets from treatment naïve patients, we found that the fraction of ADAM12+ CTLA4+ Tregs are significantly increased in patients with smoking history. Moreover, the fraction of ADAM12+ CTLA4+ Tregs are positively correlated with the fraction of exhausted T cells. Additionally, we reconstructed the spatial organization of the tumor immune microenvironment and found that ADAM12+ CTLA4+ Tregs more actively communicate with LAYN+CD8+ exhausted T cells compared with ADAM12−CTLA4+ Tregs.Our data demonstrate that smoking induced a unique subset of tumor-specific activated Tregs which interact with exhausted T cells in the TIME. Our findings not only explained how smoking impact the TIME but also provide new targets and biomarkers for precision immunotherapy of lung cancer.Yudi HuChaoqun XuJun RenYuanyuan ZengFengyang CaoHongkun FangGuo JintaoYing ZhouQiyuan LiElsevierarticleLung cancerSingle cellTumor immune microenvironmentSmokingTregNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENTranslational Oncology, Vol 15, Iss 1, Pp 101261- (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	Lung cancer Single cell Tumor immune microenvironment Smoking Treg Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Lung cancer Single cell Tumor immune microenvironment Smoking Treg Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Yudi Hu Chaoqun Xu Jun Ren Yuanyuan Zeng Fengyang Cao Hongkun Fang Guo Jintao Ying Zhou Qiyuan Li Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer
description	Tobacco smoking is the major cause of non-small-cell-lung cancer (NSCLC). However, it is barely known how smoking impact the tumor immune environment (TIME) of lung cancer.We integrated single-cell RNA-seq and bulk RNA-seq data from several studies to systematically study the impact of smoking on T cells in treatment naïve NSCLC patients. We defined a set of smoking-induced differentially expressed genes (SIDEGs) in different cells in TIME.. Specifically, we defined a smoking-related tumor-specific Treg subset, ADAM12+ CTLA4+ Tregs according to the trajectory analysis and highly express genes in cell adhesion pathways and lipid metabolism. Using independent datasets from treatment naïve patients, we found that the fraction of ADAM12+ CTLA4+ Tregs are significantly increased in patients with smoking history. Moreover, the fraction of ADAM12+ CTLA4+ Tregs are positively correlated with the fraction of exhausted T cells. Additionally, we reconstructed the spatial organization of the tumor immune microenvironment and found that ADAM12+ CTLA4+ Tregs more actively communicate with LAYN+CD8+ exhausted T cells compared with ADAM12−CTLA4+ Tregs.Our data demonstrate that smoking induced a unique subset of tumor-specific activated Tregs which interact with exhausted T cells in the TIME. Our findings not only explained how smoking impact the TIME but also provide new targets and biomarkers for precision immunotherapy of lung cancer.
format	article
author	Yudi Hu Chaoqun Xu Jun Ren Yuanyuan Zeng Fengyang Cao Hongkun Fang Guo Jintao Ying Zhou Qiyuan Li
author_facet	Yudi Hu Chaoqun Xu Jun Ren Yuanyuan Zeng Fengyang Cao Hongkun Fang Guo Jintao Ying Zhou Qiyuan Li
author_sort	Yudi Hu
title	Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer
title_short	Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer
title_full	Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer
title_fullStr	Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer
title_full_unstemmed	Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer
title_sort	exposure to tobacco smoking induces a subset of activated tumor-resident tregs in non-small cell lung cancer
publisher	Elsevier
publishDate	2022
url	https://doaj.org/article/6d02312e5664443cb9997c267a2ba995
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Exposure to Tobacco Smoking Induces a subset of Activated Tumor-resident Tregs in Non-Small Cell Lung Cancer

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