Journal
DISEASE MODELS & MECHANISMS
Volume 16, Issue 11, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dmm.050360
Keywords
Lung cancer; Mutant EGFR transgenic mice; High-fat diet; Tumor microenvironment; CRP
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High-fat diets can alter the immune microenvironment of lung cancer, promoting tumor growth, and C-reactive protein plays a significant role in this process.
To understand the effects of a high-fat diet (HFD) on lung cancer progression and biomarkers, we here used an inducible mutant epidermal growth factor receptor (EGFR)-driven lung cancer transgenic mouse model fed a regular diet (RD) or HFD. The HFD lung cancer (LC-HFD) group exhibited significant tumor formation and deterioration, such as higher EGFR activity and proliferation marker expression, compared with the RD lung cancer (LC-RD) group. Transcriptomic analysis of the lung tissues revealed that the significantly changed genes in the LC-HFD group were highly enriched in immune-related signaling pathways, suggesting that an HFD alters the immune microenvironment to promote tumor growth. Cytokine and adipokine arrays combined with a comprehensive analysis using meta-database software indicated upregulation of C reactive protein (CRP) in the LC-HFD group, which presented with increased lung cancer proliferation and metastasis; this was confirmed experimentally. Our results imply that an HFD can turn the tumor growth environment into an immune-related protumorigenic microenvironment and demonstrate that CRP has a role in promoting lung cancer development in this microenvironment.
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