Related Experiment Video
Updated: May 13, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
Complement factor B deficiency promotes lung cancer progression via FOS-mediated tryptophan metabolism and immune
Chenglu He1,2,3, Rong Gong1,2,3, Fujun Zhang4
1Department of Clinical Laboratory, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Background:
Complement Factor B (CFB) is a component of the alternative complement pathway with emerging roles in cancer biology. This study investigated the role of CFB in lung cancer progression and characterized its downstream molecular and immunological effects.
Methods:
We performed transcriptomic analysis of CFB-silenced lung adenocarcinoma cells and validated findings in clinical specimens. CFB deficiency was assessed using in vitro functional assays, metabolite measurements, and T cell coculture systems. Immunomodulatory effects were evaluated in vivo using tumor models treated with an indoleamine 2,3-dioxygenase (IDO) inhibitor.
Results:
CFB silencing activates a proto-oncogene C-Fos (FOS)-dependent upregulation of tryptophan metabolism enzymes. CFB expression inversely correlates with FOS and tryptophan metabolic enzymes in human lung cancer specimens, with stronger alterations in advanced disease. Mechanistically, CFB deficiency enhances tryptophan catabolism to kynurenine, promoting regulatory T cell activation through aryl hydrocarbon receptor (AhR) signaling while suppressing CD8 + T cell function. In vivo, CFB-knockdown tumors show accelerated growth, enhanced immune suppression, and increased tryptophan catabolism. These effects are reversed by IDO inhibitor treatment.
Conclusion:
We identify a CFB-FOS-IDO axis that regulates tryptophan metabolism and shapes the tumor immune microenvironment in lung cancer. CFB deficiency promotes tumor progression by enhancing tryptophan catabolism, resulting in an immunosuppressive microenvironment. These findings reveal potential therapeutic targets to overcome immune evasion in lung cancer.
Related Concept Videos
Other Pulmonary Disorders
Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.
Symptoms of COPD can be classified as primary or systemic. Primary symptoms relate to reduced airflow, while systemic or extrapulmonary symptoms relate to COPD's broader impact on the body.
Primary Symptoms of COPD:
Cancer Prevention
Some...
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...