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PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression
by
Wang, Tingting
, Duan, Qiongyu
, Hu, Tianyu
, Wang, Chunlei
, Wang, Yixian
, Li, Yishuo
in
cDC1
/ Immune infiltration
/ NF-κB signaling pathway
/ Non-small cell lung cancer
/ Original
/ PU.1
/ Single-cell transcriptome sequencing
2025
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PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression
by
Wang, Tingting
, Duan, Qiongyu
, Hu, Tianyu
, Wang, Chunlei
, Wang, Yixian
, Li, Yishuo
in
cDC1
/ Immune infiltration
/ NF-κB signaling pathway
/ Non-small cell lung cancer
/ Original
/ PU.1
/ Single-cell transcriptome sequencing
2025
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Do you wish to request the book?
PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression
by
Wang, Tingting
, Duan, Qiongyu
, Hu, Tianyu
, Wang, Chunlei
, Wang, Yixian
, Li, Yishuo
in
cDC1
/ Immune infiltration
/ NF-κB signaling pathway
/ Non-small cell lung cancer
/ Original
/ PU.1
/ Single-cell transcriptome sequencing
2025
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PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression
Journal Article
PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression
2025
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Overview
This research investigates the regulatory role of the transcription factor PU.1 in type 1 conventional dendritic cells (cDC1) and its therapeutic potential of modulating the nuclear factor kappaB (NF-κB) cells signaling pathway in non-small cell lung cancer (NSCLC). Utilizing single-cell transcriptome sequencing and comprehensive bioinformatics tools, including the CIBERSORT algorithm, we analyzed the immune cell landscape within NSCLC tissues. Our analysis revealed distinct NSCLC subtypes and delineated the developmental trajectories and functional distinctions of cDC1 cells. Key differentially expressed genes (DEGs) and pivotal functional modules within these cells were identified, highlighting PU.1 as a critical mediator underexpressed in NSCLC samples. Functionally, PU.1 demonstrated the induction of the NF-κB pathway, which led to inhibited tumor proliferation and enhanced activation of cDC1, thereby suggesting its role in tumor immune surveillance. In vivo models confirmed the suppressive effect of PU.1 on NSCLC progression, mediated through its influence on cDC1 functionality via the NF-κB pathway. These findings propose PU.1 as a promising target for NSCLC therapeutic strategies, emphasizing the importance of transcriptional regulators in the tumor microenvironment.
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•Revealing the critical role of cDC1 in NSCLC progression.•Identifying PU.1 as a potential regulatory gene for NSCLC for the first time.•Demonstrating that PU.1 inhibits tumor cell growth via the NF-κB pathway.•Providing a new therapeutic target for NSCLC.•Conducting in-depth analysis using single-cell transcriptome sequencing.
Publisher
Elsevier B.V,Department of Gerontology,The First Hospital of China Medical University,Shenyang,110001,China%Department of Rheumatology and Immunology,The First Hospital of China Medical University,Shenyang,110001,China%Department of Oncology,Shengjing Hospital of China Medical University,Shenyang,110022,China%Center of Reproductive Medicine,Department of Obstetrics and Gynecology,Shengjing Hospital of China Medical University,Shenyang,110022,China,Xi'an Jiaotong University,Elsevier
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