PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression.
10.1016/j.jpha.2024.101154
- Author:
Tingting WANG
1
;
Yishuo LI
2
;
Qiongyu DUAN
3
;
Chunlei WANG
1
;
Yixian WANG
4
;
Tianyu HU
3
Author Information
1. Department of Gerontology, The First Hospital of China Medical University, Shenyang, 110001, China.
2. Department of Rheumatology and Immunology, The First Hospital of China Medical University, Shenyang, 110001, China.
3. Department of Oncology, Shengjing Hospital of China Medical University, Shenyang, 110022, China.
4. Center of Reproductive Medicine, Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, 110022, China.
- Publication Type:Journal Article
- Keywords:
Immune infiltration;
NF-κB signaling pathway;
Non-small cell lung cancer;
PU.1;
Single-cell transcriptome sequencing;
cDC1
- From:
Journal of Pharmaceutical Analysis
2025;15(7):101154-101154
- CountryChina
- Language:English
-
Abstract:
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.
