Patients with
reflux esophagitis experience an increased incidence of
esophageal cancer. In China, this may be the result of contamination of the food supply by Aspergillus fungi, which is known to harbor
sterigmatocystin, a carcinogenic
mycotoxin. To delineate the potential link between
sterigmatocystin and
esophageal cancer, an experimental model of
reflux esophagitis was developed in rats that had undergone a cardiectomy and partial pylorus
ligation. The rats were treated with
sterigmatocystin or saline, and esophageal squamous cell
hyperplasia was assessed based on the pathological evaluation. The expression of
proliferating cell nuclear antigen (
PCNA), transporter associated with antigen processing 1 (TAP1) and low molecular weight
protein 2 (LMP2) was determined by immunohistochemistry. Intraperitoneal administration of
sterigmatocystin promoted the proliferation of squamous epithelium. In addition, it also increased the expression of
PCNA in esophageal epithelial cells in rats with
reflux esophagitis and was correlated with the increased severity of epithelial
hyperplasia. The expression levels of TAP1 and LMP2, which are located in the cytoplasm of esophageal epithelial cells, were reduced in rats with
reflux esophagitis, and
sterigmatocystin exposure further decreased the expression. Thus, the downregulation of TAP1 and LMP2
proteins by
sterigmatocystin may directly affect
tumor immunity by allowing transformed cells to escape the host immune surveillance, thereby promoting
esophageal cancer.