Pirfenidone inhibits TGF-β1-induced metabolic reprogramming during epithelial-mesenchymal transition in non-small cell lung cancer.

ABSTRACT: Metastasis is an important contributor to increased mortality rates in non-small cell lung cancer (NSCLC). The TGF-β signalling pathway plays a crucial role in facilitating tumour metastasis through epithelial-mesenchymal transition (EMT). Glycolysis, a key metabolic process, is strongly correlated with NSCLC metastasis. Pirfenidone (PFD) has been shown to safely and effectively inhibit TGF-β1 in patients with lung diseases. Furthermore, TGF-β1 and glycolysis demonstrate an interdependent relationship within the tumour microenvironment. Our previous study demonstrated that PFD effectively inhibited glycolysis in NSCLC cells, prompting further investigation into its potential antitumour effects in this context. Therefore, the present study aims to investigate the potential antitumour effect

SUBMITTER: Zhang S 

PROVIDER: S-EPMC10844763 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature