Nicaraven partially attenuates radiation-induced expression of adhesion molecules in the murine lung

Abstract

Thoracic irradiation has been found to promote cancer metastasis in the lungs, but the relevant mechanism remains unclear. Adhesion and extracellular matrix (ECM) molecules, major components of the tissue microenvironment, play a critical role in cancer metastasis. We have found that nicaraven, a small chemical compound, effectively protects normal tissue (stem) cells against radiation-induced injuries and attenuates cancer metastasis. In this study, we tried to investigate whether nicaraven regulates adhesion and ECM molecules expressions in the irradiated lungs. To find the potential adhesion and ECM molecules are regulated by nicaraven in the irradiated lungs, we collected the lungs from mice 24 h after thorax irradiation with a single dose of 5 Gy X-rays, and then widely evaluated the expression of adhesion and ECM molecules by RT-PCR assay. Our data showed that several adhesion and ECM molecules were up- or down-regulated in the irradiated murine lungs. Interestingly, nicaraven effectively attenuated radiation-enhanced expressions of Itga2 and Pecam1 in the murine lungs. Our study demonstrated that nicaraven suppresses the adhesion and ECM remodeling in the irradiated lungs, which may contribute to attenuate the radiation-induced enhancement of lung metastasis. Further study is warranted to determine how nicaraven regulates the expression of adhesion and ECM molecules and prevents cancer metastasis after irradiation.