Inhibition of MSB-1 cell invasion and migration by Diallyl disulfide(DADS) through NF-κB signaling pathway

Abstract

Marek's disease is a lymphoproliferative disorder in chickens characterized by monocyt Marek's disease ic infiltration of single or multiple tissues and organs of peripheral nerves, gonads, iris, various internal organs, muscles, and skin. This disease is an infectious neoplastic disease caused by cell-bound herpesvirus, which causes the formation of tumors in the above organs and tissues. Sick chickens are commonly emaciated, paralyzed, and often have acute death. To investigate the effect of diallyl disulfide (DADS) on the migration and invasion of MSB-1 cells and explore its mechanism, to lay the foundation for the study of invasion and migration of tumor cells in chicken Malik's disease. To investigate the roles of DADS on the migration and invasion of MSB-1 cells, different concentrations of DADS (0,30,90,120 µmol/L) on the growth and proliferation of MSB-1 cells was analyzed by CCK8 assay. Cell migration and invasion were detected by Transwell assays. Protein activity of related proteins MMP2 and MMP9 were detected by gelatinase profiling; the expression of related proteins NF-κB, MMP2, MMP9, VEGF, E-cadherin and Vimentin were detected by ELISA. DADS significantly inhibited the migration and invasion of MSB-1 cells and altered the morphological structure of the cells. Through data analysis, it can be concluded that the concentration of 30µmol/L DADS significantly inhibits the migration and invasion of cells, and the concentration of DADS of 60µmol/L and 90 µmol/L highly significantly inhibits the migration and invasion of cells. The expressions of migration and invasion-related proteins NF-κB, MMP2, MMP9, VEGF, E-cadherin and Vimentin were decreased in a dependent manner with increasing DADS concentration. DADS may reduce the degradation of the extracellular matrix by inhibiting the expression of MMP2 and MMP9 through suppressing the NF-κB signaling pathway, and at the same time. Might be inhibit angiogenesis by decreasing the expression of VEGF, thus inhibiting the migration and invasion of MSB-1 cells.