Idiopathic pulmonary fibrosis is a chronic, progressive, and fatal fibrotic lung disease with a poor prognosis, but no effective treatment is available. G protein-coupled receptor 56 (GPR56) plays a role in cell adhesion and tumor progression, but its function in fibrogenesis has not been explored. In this in vitro study, we found that GPR56 in IPF fibroblasts was lower than in normal fibroblasts. GPR56 regulated the production of fibronectin and type I collagen, and also changed the migratory and invasive capacity of lung fibroblasts. However, it was not sufficient to activate some classic markers of fibroblast and myofibroblast, such as α-smooth muscle actin and fibroblast specific protein 1. These findings demonstrate that reduced expression of GPR56 in lung fibroblasts may be an important link with pulmonary fibrosis, playing a role in regulating some important fibroblast functions.