Osteoglycin Inhibits the Progression of Lung Adenocarcinoma by Modulating ICAM1‐Mediated Cell Adhesion via the PI3K/AKT Pathway

ABSTRACT Lung cancer is characterized by high aggressiveness and lethality, processing in‐depth molecular mechanism investigation is particularly necessary. In our study, we found that osteoglycin (OGN) deficiency is strongly associated with a poor prognosis in lung adenocarcinoma (LUAD). OGN overexpression could inhibit the proliferation, migration, and invasion of LUAD cells. Through transcriptome sequencing analysis and experimental validation, we revealed that such OGN ‐mediated tumor suppression effect was related to cell adhesion function induced by ICAM1 downregulation, along with regulation by the PI3K/AKT signaling pathway. The present study demonstrated the specific mechanism of OGN involvement in LUAD progression, providing new evidence and potential targets for research on cancer suppression in LUAD.