Hsu, Wei-LunWei-LunHsuHsieh, Yun-TingYun-TingHsiehChen, Wei-MingWei-MingChenChien, Min-HuiMin-HuiChienLuo, Wei-JiaWei-JiaLuoChang, Jung-HsuanJung-HsuanChangDevlin, KevinKevinDevlinKANG-YI SU2023-11-242023-11-242023-11-011754-84031754-8411https://scholars.lib.ntu.edu.tw/handle/123456789/637337To 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 pro-tumorigenic microenvironment and demonstrate that CRP has a role in promoting lung cancer development in this microenvironment.enCRP; High-fat diet; Lung cancer; Mutant EGFR transgenic mice; Tumor microenvironmentjournal article10.1242/dmm.050360379297992-s2.0-85176495597https://api.elsevier.com/content/abstract/scopus_id/85176495597