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

Shangwei Xu; Chunji Chen; Hongwei Liu; Shuai Jiang; Zheng Li; Yun Wu

doi:10.1002/mc.70007

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

Mol Carcinog. 2025 Sep;64(9):1564-1579. doi: 10.1002/mc.70007. Epub 2025 Jul 13.

Authors

Shangwei Xu¹, Chunji Chen², Hongwei Liu³, Shuai Jiang¹, Zheng Li¹, Yun Wu¹

Affiliations

¹ Department of Thoracic Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai, China.
² Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
³ Department of Respiratory Medicine, Shanghai Fengxian District Central Hospital, Shanghai, China.

PMID: 40652546
DOI: 10.1002/mc.70007

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.

Keywords: cell adhesion; lung adenocarcinoma; metastasis; osteoglycin (OGN).

MeSH terms

Adenocarcinoma of Lung* / genetics
Adenocarcinoma of Lung* / metabolism
Adenocarcinoma of Lung* / pathology
Animals
Cell Adhesion
Cell Line, Tumor
Cell Movement
Cell Proliferation
Disease Progression
Female
Gene Expression Regulation, Neoplastic
Humans
Intercellular Adhesion Molecule-1* / genetics
Intercellular Adhesion Molecule-1* / metabolism
Lung Neoplasms* / genetics
Lung Neoplasms* / metabolism
Lung Neoplasms* / pathology
Male
Mice
Phosphatidylinositol 3-Kinases* / genetics
Phosphatidylinositol 3-Kinases* / metabolism
Prognosis
Proto-Oncogene Proteins c-akt* / genetics
Proto-Oncogene Proteins c-akt* / metabolism
Signal Transduction

Substances

Proto-Oncogene Proteins c-akt
Phosphatidylinositol 3-Kinases
Intercellular Adhesion Molecule-1
ICAM1 protein, human

Grants and funding

This study was supported by Huadong Hospital Affiliated to Fudan University, Wu Jieping Medical Foundation and National Nature Cultivation Youth Project.