Abstract 2353: PTGES is involved in the myofibroblast differentiation

Abstract Lung cancer is the leading cause of cancer-related death worldwide, and patients usually have poor prognoses and low 5-year survival rates. Idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) are both chronic and dysfunction of lung refers to lung fibrosis and increased risk of lung cancer. Myofibroblasts contribute to the procession of asthma, COPD, and IPF, leading to fibrosis of the airway and lung. Accumulating evidence has shown metabolic reprogramming has been considered a major hallmark of fibrosis and plays an important role in the fibrosis process. In this study, we identified Prostaglandin E Synthase (PTGES) was upregulated in lung fibroblast after being treated with IL-4, IL-13, and TNF-α, respectively. We found that PTGES increased the levels of myofibroblast markers α-SMA, FAP, and Vimentin, and promoted lung fibroblast cell migration and invasion. Further, in vivo lung fibrosis model demonstrated that PTGES was upregulated in lung fibrosis rats. PTGES induces phosphorylation of ERK1/2 and HIF-1α expression in lung fibroblast cells. Based on our findings, PTGES increases the expression of myofibroblast markers to modulate the myofibroblast differentiation. Citation Format: Yi-Fang Yang, Yi-Chen Lee, Min-Hsi Lin. PTGES is involved in the myofibroblast differentiation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2353.