ABI3BP can inhibit the proliferation, invasion, and epithelial-mesenchymal transition of non-small-cell lung cancer cells.

Abstract

Lung cancer, especially non-small-cell lung cancer (NSCLC), has a poor 5-year survival rate below 20%, with factors like smoking, air pollution, and genetic mutations contributing to its development. ABI3BP, an extracellular matrix protein, inhibits NSCLC progression by regulating key signaling pathways; however, its exact mechanisms remain elusive. This study aimed to explore ABI3BP's role in NSCLC and its impact on these pathways. We found that ABI3BP expression was significantly reduced in NSCLC cells compared to normal controls. Overexpression of ABI3BP in NSCLC cells resulted in a substantial reduction in cell growth and motility and induced cell cycle arrest. Furthermore, its overexpression suppressed the epithelial-mesenchymal transition (EMT) process in NSCLC cells. In addition, ABI3BP overexpression inhibited the MAPK/ERK pathway in NSCLC cells. Collectively, ABI3BP functions as a tumor suppressor in NSCLC by targeting the MAPK/ERK axis, thereby regulating cell proliferation, motility, and EMT. These findings suggest that ABI3BP represents a potential therapeutic target for NSCLC treatment.