Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer

Abstract Lung cancer is one of the most commonly diagnosed cancers worldwide and the leading cause of cancer-related deaths worldwide. In recent years, an increasing number of studies have shown that the tumor immune microenvironment (TIME) has a significant impact on the development of lung cancer....

Full description

Saved in:
Bibliographic Details
Main Authors: Huan Cheng, Yajiao Shao, Ao Zhang, Caixia Li, Xinxin Li, Yuxin Fu, Jian Ming
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Scientific Reports
Subjects:
Online Access:https://doi.org/10.1038/s41598-025-01868-5
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849333104668311552
author Huan Cheng
Yajiao Shao
Ao Zhang
Caixia Li
Xinxin Li
Yuxin Fu
Jian Ming
author_facet Huan Cheng
Yajiao Shao
Ao Zhang
Caixia Li
Xinxin Li
Yuxin Fu
Jian Ming
author_sort Huan Cheng
collection DOAJ
description Abstract Lung cancer is one of the most commonly diagnosed cancers worldwide and the leading cause of cancer-related deaths worldwide. In recent years, an increasing number of studies have shown that the tumor immune microenvironment (TIME) has a significant impact on the development of lung cancer. Interleukin-7 (IL-7) is an essential cytokine for the adaptive immune system and plays an important immunoregulatory role in different types of tumors. However, the relationship between IL-7 and TIME in non-small cell lung cancer (NSCLC) is not yet known. This study found that the expression of MCP-1 and CD11b was correlated with the expression of IL-7/IL-7R. MCP-1, IL-7R, tumor differentiation and tumor stage were the strongest predictors of survival. In addition, IL-7 upregulates MCP-1 through JAK1/STAT3 pathway to affect the migration of MDSCs and exert tumor immunosuppressive effect. Furthermore, CCR2 inhibitor and depletion of MDSCs suppressed the promoting effect of IL-7 mediated development of lung cancer. These findings provided the important mechanism that IL-7 upregulate MCP-1 through JAK1/STAT3 pathway to recruit MDSCs and put forth blockage of CCR2 inhibitor and MDSCs recruitment as a prospective immunotherapy strategy for the treatment of NSCLC.
format Article
id doaj-art-290817292c03460f93dee8e9aad9aecd
institution Kabale University
issn 2045-2322
language English
publishDate 2025-05-01
publisher Nature Portfolio
record_format Article
series Scientific Reports
spelling doaj-art-290817292c03460f93dee8e9aad9aecd2025-08-20T03:45:59ZengNature PortfolioScientific Reports2045-23222025-05-0115111710.1038/s41598-025-01868-5Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancerHuan Cheng0Yajiao Shao1Ao Zhang2Caixia Li3Xinxin Li4Yuxin Fu5Jian Ming6Department of Pathology, General Hospital of Northern Theater CommandDepartment of Pathology, General Hospital of Northern Theater CommandDepartment of Pathology, General Hospital of Northern Theater CommandDepartment of Pathology, General Hospital of Northern Theater CommandDepartment of Pathology, General Hospital of Northern Theater CommandDepartment of Pathology, General Hospital of Northern Theater CommandDepartment of Pathology, General Hospital of Northern Theater CommandAbstract Lung cancer is one of the most commonly diagnosed cancers worldwide and the leading cause of cancer-related deaths worldwide. In recent years, an increasing number of studies have shown that the tumor immune microenvironment (TIME) has a significant impact on the development of lung cancer. Interleukin-7 (IL-7) is an essential cytokine for the adaptive immune system and plays an important immunoregulatory role in different types of tumors. However, the relationship between IL-7 and TIME in non-small cell lung cancer (NSCLC) is not yet known. This study found that the expression of MCP-1 and CD11b was correlated with the expression of IL-7/IL-7R. MCP-1, IL-7R, tumor differentiation and tumor stage were the strongest predictors of survival. In addition, IL-7 upregulates MCP-1 through JAK1/STAT3 pathway to affect the migration of MDSCs and exert tumor immunosuppressive effect. Furthermore, CCR2 inhibitor and depletion of MDSCs suppressed the promoting effect of IL-7 mediated development of lung cancer. These findings provided the important mechanism that IL-7 upregulate MCP-1 through JAK1/STAT3 pathway to recruit MDSCs and put forth blockage of CCR2 inhibitor and MDSCs recruitment as a prospective immunotherapy strategy for the treatment of NSCLC.https://doi.org/10.1038/s41598-025-01868-5IL-7MDSCsMCP-1NSCLC
spellingShingle Huan Cheng
Yajiao Shao
Ao Zhang
Caixia Li
Xinxin Li
Yuxin Fu
Jian Ming
Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer
Scientific Reports
IL-7
MDSCs
MCP-1
NSCLC
title Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer
title_full Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer
title_fullStr Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer
title_full_unstemmed Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer
title_short Interleukin-7 enhances recruitment of MDSCs by regulating MCP-1 via JAK1/STAT3 signaling pathway in non-small cell lung cancer
title_sort interleukin 7 enhances recruitment of mdscs by regulating mcp 1 via jak1 stat3 signaling pathway in non small cell lung cancer
topic IL-7
MDSCs
MCP-1
NSCLC
url https://doi.org/10.1038/s41598-025-01868-5
work_keys_str_mv AT huancheng interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer
AT yajiaoshao interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer
AT aozhang interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer
AT caixiali interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer
AT xinxinli interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer
AT yuxinfu interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer
AT jianming interleukin7enhancesrecruitmentofmdscsbyregulatingmcp1viajak1stat3signalingpathwayinnonsmallcelllungcancer