Gene expression profiling analysis of deoxynivalenol-induced inhibition of mouse thymic epithelial cell proliferation

- Deoxynivalenol (DON) can induce cytotoxicity in MTEC1 cells.
- DON can inhibit the proliferation of MTEC1 cells through G1 phase arrest.
- P53 signaling pathway may play an important role in the proliferation inhibition of MTEC1 cells.

Deoxynivalenol (DON) is a mycotoxin produced as a secondary metabolite by fungal species. It has been shown that DON has serious toxic effects on many kinds of immune cells. However, the toxic effects on thymic epithelial cells were poorly understood. The purpose of this study is to investigate the gene expression differences for the DON-induced inhibition on the proliferation of mouse thymic epithelial cell line 1 (MTEC1). After the experiments of cell viability, morphological investigation and cell cycle analysis, microarray analysis was carried out. The differentially expressed genes belong to a variety of functional categories, including genes involved in metabolic process, cell cycle, oxidation-reduction process and apoptosis. Our results provide molecular insights into the gene expression differences of DON-induced toxic effects and suggest that p53 signaling pathway may play an important role in the inhibition of MTEC1 cell proliferation.