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MIF-Associated Immunosuppressive CAF Remodeling Predicts Poor Prognosis During Lung Adenocarcinoma Progression: A
Guo Lin1, Jianrui Ji1, Fan Ge2
1Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Biomedicines
|July 28, 2026
Summary
Cancer-associated fibroblasts (CAFs) remodel the tumor microenvironment during lung adenocarcinoma (LUAD) progression, contributing to immune suppression. A new MIF-related gene signature aids in prognostic stratification for LUAD patients.
Area of Science:
- Oncology
- Immunology
- Bioinformatics
Background:
- Lung adenocarcinoma (LUAD) progresses through distinct pathological stages from atypical adenomatous hyperplasia (AAH) to invasive adenocarcinoma (IA).
- The role of cancer-associated fibroblasts (CAFs) and their impact on the immunosuppressive tumor microenvironment (TME) during LUAD progression are not fully understood.
Purpose of the Study:
- To characterize CAF subtypes and their dynamic remodeling across LUAD pathological stages.
- To investigate epithelial-CAF communication, particularly MIF-related signaling.
- To develop and validate a prognostic signature based on MIF-related genes for LUAD.
Main Methods:
- Single-cell RNA sequencing of treatment-naïve LUAD lesions (AAH, AIS, MIA, IA).
- Analysis of CAF subsets' transcriptional features, developmental states, and cell-cell interactions.
- Ligand-receptor analysis for MIF-related communication; machine learning model for prognostic signature development and validation.
Main Results:
- Six CAF subtypes identified; CAF composition varied across pathological stages, with MIA showing eCAF enrichment.
- Invasive adenocarcinoma (IA) exhibited increased exhausted T cells and enhanced epithelial-CAF interactions, including MIF-CD74/CD44 signaling.
- A validated machine learning prognostic signature based on MIF-related genes stratified LUAD patients by survival outcomes.
Conclusions:
- CAF-driven stromal remodeling is linked to immune suppression during LUAD progression.
- MIF-mediated epithelial-CAF communication may drive an immunosuppressive TME and is associated with poor prognosis.
- The developed MIF-related signature shows potential for prognostic stratification in LUAD.